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1
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0030006070
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Clonal selection and learning in the antibody system
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Rajewsky K. Clonal selection and learning in the antibody system. Nature. 381:1996;751-758.
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Nature
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Rajewsky, K.1
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2
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0026652354
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A critical role of λ5 protein in B cell development
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Kitamura D, Kudo A, Schaal S, Muller W, Melchers F, Rajewsky K. A critical role of λ5 protein in B cell development. Cell. 69:1992;823-831.
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Kitamura, D.1
Kudo, A.2
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Melchers, F.5
Rajewsky, K.6
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3
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0025852445
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A B cell-deficient mouse by targeted disruption of the membrane exon of the immunoglobulin μ chain gene
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Kitamura D, Roes J, Kuhn R, Rajewsky K. A B cell-deficient mouse by targeted disruption of the membrane exon of the immunoglobulin μ chain gene. Nature. 350:1991;423-425.
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Kitamura, D.1
Roes, J.2
Kuhn, R.3
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0029913115
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Regulation of an early developmental checkpoint in the B cell pathway by Ig beta
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Gong S, Nussensweig MC. Regulation of an early developmental checkpoint in the B cell pathway by Ig beta. Science. 272:1996;411-414.
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Gong, S.1
Nussensweig, M.C.2
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5
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0342711256
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In vivo ablation of surface immunoglobulin on mature B cells by inducible gene targeting results in rapid cell death
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of outstanding interest. This study was a technical and conceptual tour de force. Mice harboring a Cre recombinase transgene under the control of a type I interferon-inducible promoter were crossed with mice expressing a BCR transgene specific for the hapten 4-hydroxy-3-nitrophenyl acetyl (NP). Treatment of these mice with recombinant α/β interferon ablated expression of the transgenic BCR through activation of Cre recombinase. The so-called 'receptorless' B cells underwent apoptosis in vivo, and cell death could be delayed, but not prevented, by constitutive expression of Bcl-2. The study provides powerful support for the argument that signaling through the BCR is essential for survival, although the biophysical nature of the cross-linking event or the biochemical nature of the signaling event in this model is unknown. It is unlikely that a naturally occurring in vivo 'NP homologue' was responsible for BCR cross-linking.
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of outstanding interest Lam KP, Kühn R, Rajewsky K. In vivo ablation of surface immunoglobulin on mature B cells by inducible gene targeting results in rapid cell death. Cell. 90:1997;1073-1083 This study was a technical and conceptual tour de force. Mice harboring a Cre recombinase transgene under the control of a type I interferon-inducible promoter were crossed with mice expressing a BCR transgene specific for the hapten 4-hydroxy-3-nitrophenyl acetyl (NP). Treatment of these mice with recombinant α/β interferon ablated expression of the transgenic BCR through activation of Cre recombinase. The so-called 'receptorless' B cells underwent apoptosis in vivo, and cell death could be delayed, but not prevented, by constitutive expression of Bcl-2. The study provides powerful support for the argument that signaling through the BCR is essential for survival, although the biophysical nature of the cross-linking event or the biochemical nature of the signaling event in this model is unknown. It is unlikely that a naturally occurring in vivo 'NP homologue' was responsible for BCR cross-linking.
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(1997)
Cell
, vol.90
, pp. 1073-1083
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Lam, K.P.1
Kühn, R.2
Rajewsky, K.3
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6
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0030886340
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Antigen receptor signaling gives lymphocytes a long life
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of outstanding interest. This minireview provides insightful comment on the study by Lam and colleagues [5], and discusses differing states of BCR signaling, culminating in preservation of B cell survival or antigen-driven B cell activation.
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of outstanding interest Neuberger MS. Antigen receptor signaling gives lymphocytes a long life. Cell. 90:1997;971-973 This minireview provides insightful comment on the study by Lam and colleagues [5], and discusses differing states of BCR signaling, culminating in preservation of B cell survival or antigen-driven B cell activation.
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(1997)
Cell
, vol.90
, pp. 971-973
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Neuberger, M.S.1
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7
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0023035608
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λ5, a new light-chain-related locus selectively expressed in pre-B lymphocytes
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Sakaguchi N, Melchers F. λ5, a new light-chain-related locus selectively expressed in pre-B lymphocytes. Nature. 324:1986;579-582.
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(1986)
Nature
, vol.324
, pp. 579-582
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Sakaguchi, N.1
Melchers, F.2
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8
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0031066917
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Down-regulation of terminal deoxynucleotidyl transferase by Ig heavy chain in B lineage cells
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Wasserman R, Li Y-S, Hardy RR. Down-regulation of terminal deoxynucleotidyl transferase by Ig heavy chain in B lineage cells. J Immunol. 158:1997;1133-1138.
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(1997)
J Immunol
, vol.158
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Wasserman, R.1
Li Y-S2
Hardy, R.R.3
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9
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0030765923
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H gene repertoire of developing precursor B lymphocytes in mouse bone marrow mediated by the pre-B cell receptor
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- large pre-B-II cells. The authors concluded that the pre-BCR mediates this repertoire shift, although it is unclear whether this shift occurs by a signaling mechanism transduced through the pre-BCR.
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- large pre-B-II cells. The authors concluded that the pre-BCR mediates this repertoire shift, although it is unclear whether this shift occurs by a signaling mechanism transduced through the pre-BCR.
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(1997)
Immunity
, vol.7
, pp. 357-368
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Ten Boekel, E.1
Melchers, F.2
Rolink, A.G.3
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10
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0031569221
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Secretion of soluble pre-B cell receptors by pre-B cells
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Bornemann KD, Brewer JW, Perez E, Doerre S, Sita R, Corley RB. Secretion of soluble pre-B cell receptors by pre-B cells. J Immunol. 158:1997;2551-2557.
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(1997)
J Immunol
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Bornemann, K.D.1
Brewer, J.W.2
Perez, E.3
Doerre, S.4
Sita, R.5
Corley, R.B.6
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12
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0031203032
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A truncated heavy chain protein relieves the requirement for surrogate light chains in early B cell development
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H and CH1, as well as half of the CH2 domain; the other with a full-length human μ transgene. Both strains were bred onto a recombination-activating gene (RAG)-1-deficient background. The full-length human μ HC protein could not be detected on the surface of RAG-1 deficient/μ-transgenic B-lineage cells, whereas the truncated murine μ HC protein was readily detected. It was assumed that the full-length human μ HC associated with murine SLC, although direct evidence was not presented
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H and CH1, as well as half of the CH2 domain; the other with a full-length human μ transgene. Both strains were bred onto a recombination-activating gene (RAG)-1-deficient background. The full-length human μ HC protein could not be detected on the surface of RAG-1 deficient/μ-transgenic B-lineage cells, whereas the truncated murine μ HC protein was readily detected. It was assumed that the full-length human μ HC associated with murine SLC, although direct evidence was not presented. The truncated murine μ HC protein was expressed on the surface without SLC. Remarkably, B-lineage cells expressing truncated murine μ HC underwent developmental changes (i.e. changes in surface markers, transcriptional regulation, and recombinase retargeting) indistinguishable from those occurring in mice expressing full-length human μ HC. A thoughtful discussion considered the ramifications of results obtained in these genetically altered mice, and argued for a chaperone function as the primary role for SLC in the function of the pre-BCR.
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(1997)
J Immunol
, vol.159
, pp. 1265-1275
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Shaffer, A.L.1
Schlissel, M.S.2
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13
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0030611753
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The Igα/Igβ heterodimer on μ-negative proB cells is competent for transducing signals to induce early B cell differentiation
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of outstanding interest. The authors used pro-B cell lines and early B-lineage cells from recombination-activating gene-2-deficient mice to identify stable cell-surface complexes consisting of the Ig-α/Ig-β signaling heterodimer and the molecular chaperone calnexin. At least some of the Ig-α/Ig-β complexes did not contain μ heavy chain (HC) or surrogate light chain (SLC). An in-depth series of experiments confirmed that cross-linking Ig-β on these cells induced the tyrosine phosphorylation of several intracellular signaling proteins (e.g. Syk, PI-3 kinase, ERK) in vitro and induced pro-B to pre-B cell differentiation in vivo. It remains to be determined, however, whether Ig-α/Ig-β complexes devoid of μ HC and SLC exist on the surface of pro-B cells in normal mice.
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of outstanding interest Nagata K, Nakamura T, Kitamura F, Kuramochi S, Taki S, Campbell KS, Karasuyama H. The Igα/Igβ heterodimer on μ-negative proB cells is competent for transducing signals to induce early B cell differentiation. Immunity. 7:1997;559-570 The authors used pro-B cell lines and early B-lineage cells from recombination-activating gene-2-deficient mice to identify stable cell-surface complexes consisting of the Ig-α/Ig-β signaling heterodimer and the molecular chaperone calnexin. At least some of the Ig-α/Ig-β complexes did not contain μ heavy chain (HC) or surrogate light chain (SLC). An in-depth series of experiments confirmed that cross-linking Ig-β on these cells induced the tyrosine phosphorylation of several intracellular signaling proteins (e.g. Syk, PI-3 kinase, ERK) in vitro and induced pro-B to pre-B cell differentiation in vivo. It remains to be determined, however, whether Ig-α/Ig-β complexes devoid of μ HC and SLC exist on the surface of pro-B cells in normal mice.
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(1997)
Immunity
, vol.7
, pp. 559-570
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Nagata, K.1
Nakamura, T.2
Kitamura, F.3
Kuramochi, S.4
Taki, S.5
Campbell, K.S.6
Karasuyama, H.7
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14
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0027182253
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A complex of glycoproteins is associated with VpreB/λ5 surrogate light chain on the surface of μ heavy chain-negative early precursor B cell lines
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Karasuyama H, Rolink A, Melchers F. A complex of glycoproteins is associated with VpreB/λ5 surrogate light chain on the surface of μ heavy chain-negative early precursor B cell lines. J Exp Med. 178:1993;469-478.
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(1993)
J Exp Med
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Karasuyama, H.1
Rolink, A.2
Melchers, F.3
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15
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0029930417
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Assembly of the truncated immunoglobulin heavy chain Dμ into antigen receptor-like complexes in pre-B cells but not in B cells
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Horne MC, Roth PE, DeFranco AL. Assembly of the truncated immunoglobulin heavy chain Dμ into antigen receptor-like complexes in pre-B cells but not in B cells. Immunity. 4:1996;145-158.
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Immunity
, vol.4
, pp. 145-158
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Horne, M.C.1
Roth, P.E.2
Defranco, A.L.3
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16
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0343812092
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IL-7 receptor and VDJ recombination: Trophic versus mechanistic actions
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Candeias S, Muegge SK, Durum S. IL-7 receptor and VDJ recombination: trophic versus mechanistic actions. Immunity. 6:1997;501-508.
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(1997)
Immunity
, vol.6
, pp. 501-508
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Candeias, S.1
Muegge, S.K.2
Durum, S.3
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17
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0030787787
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Bcl-2 rescues T lymphopoiesis, but not B or NK cell development, in common γ chain-deficient mice
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of special interest. This study crossed mice deficient in the common γ chain subunit of the IL-2/-4/-7/-9/-15 receptors with mice expressing a Bcl-2 transgene under the control of the Eμ or H2K promoters. The forced expression of Bcl-2 led to a significant, albeit incomplete, restoration of thymocyte expansion and thymic positive selection, but had no detectable effect on B-cell or natural killer-cell development. These data argue that signaling through, for example, the IL-7 receptor α chain/γ chain complex may lead to different survival outcomes in individual lymphoid lineages.
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of special interest Kondo M, Akashi K, Domen J, Sugamura K, Weissman IL. Bcl-2 rescues T lymphopoiesis, but not B or NK cell development, in common γ chain-deficient mice. Immunity. 7:1997;155-162 This study crossed mice deficient in the common γ chain subunit of the IL-2/-4/-7/-9/-15 receptors with mice expressing a Bcl-2 transgene under the control of the Eμ or H2K promoters. The forced expression of Bcl-2 led to a significant, albeit incomplete, restoration of thymocyte expansion and thymic positive selection, but had no detectable effect on B-cell or natural killer-cell development. These data argue that signaling through, for example, the IL-7 receptor α chain/γ chain complex may lead to different survival outcomes in individual lymphoid lineages.
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(1997)
Immunity
, vol.7
, pp. 155-162
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Kondo, M.1
Akashi, K.2
Domen, J.3
Sugamura, K.4
Weissman, I.L.5
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18
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0031587826
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Bcl-2 rescues T lymphpoiesis in interleukin-7 receptor-deficient mice
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Akashi K, Kondo M, von Freeden-Jeffry U, Murray R, Weissman IL. Bcl-2 rescues T lymphpoiesis in interleukin-7 receptor-deficient mice. Cell. 89:1997;1033-1041.
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(1997)
Cell
, vol.89
, pp. 1033-1041
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Akashi, K.1
Kondo, M.2
Von Freeden-Jeffry, U.3
Murray, R.4
Weissman, I.L.5
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20
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0030939476
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Constitutive bcl-2 expression during immunoglobulin heavy chain-promoted B cell differentiation expands novel precursor B cells
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of special interest. The potential cooperativity of Bcl-2 and μ heavy chain (HC) in mediating survival, proliferation or differentiation of B cell precursors was examined. The Bcl-2 and μ HC transgenes were introduced individually, or together, into recombination-activating gene-2-deficient mice. Bcl-2 alone promoted expansion, but not differentiation, of pro-B cells (that, somewhat surprisingly, was more marked in spleen than bone marrow). On the other hand, the μHC transgene promoted pro-B to pre-B differentiation as assessed by acquisition of CD22 and low-level surface μ. This effect was enhanced by co-expression of the Bcl-2 transgene. The pre-B cells in the Bcl-2/μ HC double transgenics exhibited somewhat of a precocious immature B-cel phenotype, as assessed
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of special interest Young F, Mizoguchi E, Bhan AK, Alt FW. Constitutive bcl-2 expression during immunoglobulin heavy chain-promoted B cell differentiation expands novel precursor B cells. Immunity. 6:1997;23-33 The potential cooperativity of Bcl-2 and μ heavy chain (HC) in mediating survival, proliferation or differentiation of B cell precursors was examined. The Bcl-2 and μ HC transgenes were introduced individually, or together, into recombination-activating gene-2-deficient mice. Bcl-2 alone promoted expansion, but not differentiation, of pro-B cells (that, somewhat surprisingly, was more marked in spleen than bone marrow). On the other hand, the μHC transgene promoted pro-B to pre-B differentiation as assessed by acquisition of CD22 and low-level surface μ. This effect was enhanced by co-expression of the Bcl-2 transgene. The pre-B cells in the Bcl-2/μ HC double transgenics exhibited somewhat of a precocious immature B-cel phenotype, as assessed by unexpectedly high cell-surface levels of CD21, CD22, CD23 and CD40. This interesting Bcl-2/μ HC double transgenic may have revealed a rare population of transient cells at the pre-B to immature B cell interface.
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(1997)
Immunity
, vol.6
, pp. 23-33
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Young, F.1
Mizoguchi, E.2
Bhan, A.K.3
Alt, F.W.4
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21
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0030608977
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Continued differentiation during B lymphopoiesis requires signals in addition to cell survival
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Tarlinton DM, Corcoran LM, Strasser A. Continued differentiation during B lymphopoiesis requires signals in addition to cell survival. Int Immunol. 9:1997;1481-1494.
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(1997)
Int Immunol
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Tarlinton, D.M.1
Corcoran, L.M.2
Strasser, A.3
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22
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0031230361
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Expression of a bcl-2 transgene reduces proliferation and slows turnover of developing B lymphocytes in vivo
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O'Reilly LA, Harris AW, Tarlinton DM, Corcoran LM, Strasser A. Expression of a bcl-2 transgene reduces proliferation and slows turnover of developing B lymphocytes in vivo. J Immunol. 159:1997;2301-2311.
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(1997)
J Immunol
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O'Reilly, L.A.1
Harris, A.W.2
Tarlinton, D.M.3
Corcoran, L.M.4
Strasser, A.5
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23
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0028929565
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Lymphopenia in interleukin (IL)-7 gene-deleted mice identifies IL-7 as a nonredundant cytokine
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Von Freeden-Jeffry U, Vieira P, Lucian LA, McNeil T, Burdach SE, Murray R. Lymphopenia in interleukin (IL)-7 gene-deleted mice identifies IL-7 as a nonredundant cytokine. J Exp Med. 181:1995;1519-1526.
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Von Freeden-Jeffry, U.1
Vieira, P.2
Lucian, L.A.3
McNeil, T.4
Burdach, S.E.5
Murray, R.6
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24
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0031985281
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Impaired ability of bone marrow stromal cells to support B-lymphopoiesis with age
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Stephan RP, Reilly CR, Witte PL. Impaired ability of bone marrow stromal cells to support B-lymphopoiesis with age. Blood. 91:1998;75-88.
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Stephan, R.P.1
Reilly, C.R.2
Witte, P.L.3
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25
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0031568406
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Development of B cells in aged mice: Decline in the ability of pro-B cells to respond to IL-7 but not to other growth factors
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Stephan RP, Lill-Elghanian DA, Witte PL. Development of B cells in aged mice: decline in the ability of pro-B cells to respond to IL-7 but not to other growth factors. J Immunol. 158:1997;1598-1609.
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(1997)
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Stephan, R.P.1
Lill-Elghanian, D.A.2
Witte, P.L.3
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26
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0024392322
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Interleukin 7 production and function in stromal cell-dependent B cell development
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Sudo T, Ito M, Oyawa Y, Iizuka M, Kodama H, Kunisoda T, Hayaski SI, Ogawa M, Sakai K, Nishikawa S, Nishikawa SI. Interleukin 7 production and function in stromal cell-dependent B cell development. J Exp Med. 170:1989;333-338.
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Sudo, T.1
Ito, M.2
Oyawa, Y.3
Iizuka, M.4
Kodama, H.5
Kunisoda, T.6
Hayaski, S.I.7
Ogawa, M.8
Sakai, K.9
Nishikawa, S.10
Nishikawa, S.I.11
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0029049437
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Stimulation of human bone marrow stromal cell tyrosine kinases and IL-6 production by contact with B lymphocytes
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Jarvis LJ, LeBien TW. Stimulation of human bone marrow stromal cell tyrosine kinases and IL-6 production by contact with B lymphocytes. J Immunol. 155:1995;2359-2368.
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Jarvis, L.J.1
Lebien, T.W.2
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0031183022
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TGF-β down-regulates stromal IL-7 secretion and inhibits proliferation of human B cell precursors
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Tang J, Nuccie BL, Ritterman I, Liesveld JL, Abboud CN, Ryan DH. TGF-β down-regulates stromal IL-7 secretion and inhibits proliferation of human B cell precursors. J Immunol. 159:1997;117-125.
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Tang, J.1
Nuccie, B.L.2
Ritterman, I.3
Liesveld, J.L.4
Abboud, C.N.5
Ryan, D.H.6
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Interleukin 7 independent development of human B cells
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Pribyl, J.A.1
Lebien, T.W.2
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30
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0029151210
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Immunoglobulin recombinase gene activity is modulated reciprocally by interleukin 7 and CD19 in B cell progenitors
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Billips LG, Nunez CA, Bertrand FE III, Stankovic AK, Gartland GL, Burrows PD, Cooper MD. Immunoglobulin recombinase gene activity is modulated reciprocally by interleukin 7 and CD19 in B cell progenitors. J Exp Med. 182:1995;973-982.
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Billips, L.G.1
Nunez, C.A.2
Bertrand F.E. III3
Stankovic, A.K.4
Gartland, G.L.5
Burrows, P.D.6
Cooper, M.D.7
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31
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0031201060
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A functional B cell receptor transgene allows efficient IL-7-independent maturation of B cell precursors
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Melamed D, Kench JA, Grabstein K, Rolink A, Nemazee D. A functional B cell receptor transgene allows efficient IL-7-independent maturation of B cell precursors. J Immunol. 159:1997;1233-1239.
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J Immunol
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Melamed, D.1
Kench, J.A.2
Grabstein, K.3
Rolink, A.4
Nemazee, D.5
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The influence of IL-7 V(D)J recombination
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Dobbeling U. The influence of IL-7 V(D)J recombination. Immunology. 89:1996;569-572.
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Immunology
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Dobbeling, U.1
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33
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0030029570
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The Flk2/Flt3 ligand synergizes with interleukin-7 in promoting stromal-cell-independent expansion and differentiation of human fetal pro-B cells in vitro
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Namikawa R, Muench MO, De Vries JE, Roncarolo M-G. The Flk2/Flt3 ligand synergizes with interleukin-7 in promoting stromal-cell-independent expansion and differentiation of human fetal pro-B cells in vitro. Blood. 87:1996;1881-1890.
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Namikawa, R.1
Muench, M.O.2
De Vries, J.E.3
Roncarolo M-G4
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34
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0030849638
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The role of mel-18, a mammalian polycomb group gene, during IL-7-dependent proliferation of lymphocyte precursors
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of special interest. This intriguing paper introduces Polycomb group (Pc-G) gene function into the IL-7 proliferation equation. Pc-G genes in Drosophila melanogaster are transcription factors that regulate expression of HOM-C genes, which in turn are induced by segmentation gene products such as Kruppel and hunchback. The outcome of these complex interactions includes the determination of anterior-posterior segment identity in the fly. Vertebrate homologs of Pc-G have been identified, and include mel-18 and bmi-1. Evidence from several laboratories suggested a possible role for bmi-1 in hematopoietic cell proliferation. The current study examined lymphoid growth in mel-18-deficient mice. In addition to skeletal and smooth muscle abnormalities, mel-18-deficient mice exhibited defects in B-cell and T-cell lymphopoiesis that resembled the defects which occur in IL-7-deficient
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of rest Akusaka T, Tsuji K-I, Kawakira H, Kanno M, Harigaya K-I, Hu L, Ebihara Y, Nakahata T, Tetsu O, Taniguchi M, Koseki H. The role of mel-18, a mammalian polycomb group gene, during IL-7-dependent proliferation of lymphocyte precursors. Immunity. 7:1997;135-146 This intriguing paper introduces Polycomb group (Pc-G) gene function into the IL-7 proliferation equation. Pc-G genes in Drosophila melanogaster are transcription factors that regulate expression of HOM-C genes, which in turn are induced by segmentation gene products such as Kruppel and hunchback. The outcome of these complex interactions includes the determination of anterior-posterior segment identity in the fly. Vertebrate homologs of Pc-G have been identified, and include mel-18 and bmi-1. Evidence from several laboratories suggested a possible role for bmi-1 in hematopoietic cell proliferation. The current study examined lymphoid growth in mel-18-deficient mice. In addition to skeletal and smooth muscle abnormalities, mel-18-deficient mice exhibited defects in B-cell and T-cell lymphopoiesis that resembled the defects which occur in IL-7-deficient mice. IL-7-dependent proliferation of thymocytes and pre-B-cell colony formation were reduced in mel-18-deficient mice; however, analysis of the expression and function of IL-7 signaling pathway molecules (γ chain, Jak3, STATS) revealed no detectable deficiencies in mel-18-deficient mice. Thus, mel-18 is important in IL-7 dependent proliferation, but acts potentially downstream of, or parallel to, Jak/STAT function.
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(1997)
Immunity
, vol.7
, pp. 135-146
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Akusaka, T.1
Tsuji K-I2
Kawakira, H.3
Kanno, M.4
Harigaya K-I5
Hu, L.6
Ebihara, Y.7
Nakahata, T.8
Tetsu, O.9
Taniguchi, M.10
Koseki, H.11
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35
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0030834968
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Matrix glycoprotein SC1/ECM2 augments B lymphopoiesis
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of special interest. Oritani and Kincade have previously developed a novel cloning strategy that selects for stromal cell molecules that bind to the surface of pre-B cells. This study confirms the utility of that cloning strategy, by demonstrating that secreted and membrane forms of a matrix glycoprotein designated SC1/ECM2 can potentiate the clonogenicity of IL-7-dependent pre-B cells.
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of special interest Oritani K, Kanakura Y, Aoyama K, Yokota T, Copeland NG, Gilbert DJ, Jenkins NA, Tomiyama Y, Matsuzawa Y, Kincade PW. Matrix glycoprotein SC1/ECM2 augments B lymphopoiesis. Blood. 90:1997;3404-3413 Oritani and Kincade have previously developed a novel cloning strategy that selects for stromal cell molecules that bind to the surface of pre-B cells. This study confirms the utility of that cloning strategy, by demonstrating that secreted and membrane forms of a matrix glycoprotein designated SC1/ECM2 can potentiate the clonogenicity of IL-7-dependent pre-B cells.
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(1997)
Blood
, vol.90
, pp. 3404-3413
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Oritani, K.1
Kanakura, Y.2
Aoyama, K.3
Yokota, T.4
Copeland, N.G.5
Gilbert, D.J.6
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Molecular cloning and structure of a pre-B-cell growth-stimulating factor
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37
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The chemokine SDF-1, stromal cell-derived factor 1, attracts early stage B cell precursors via the chemokine receptor CXCR4
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+ population, CD19- (i.e., Hardy fraction A) cells exhibited the strongest chemotactic response to SDF-1. Analysis of human pro-B leukemic, pre-B leukemic and Burkitt lymphoma cell lines revealed both a chemotactic response and a transient rise in intracellular calcium response to SDF-1 in the pro-B and pre-B cells. Importantly, an antibody to the CXCR4 chemokine receptor for SDF-1 blocked migration. This report provides the first evidence that B cell precursors exhibit chemotactic responses to a specific chemokine.
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+ population, CD19- (i.e., Hardy fraction A) cells exhibited the strongest chemotactic response to SDF-1. Analysis of human pro-B leukemic, pre-B leukemic and Burkitt lymphoma cell lines revealed both a chemotactic response and a transient rise in intracellular calcium response to SDF-1 in the pro-B and pre-B cells. Importantly, an antibody to the CXCR4 chemokine receptor for SDF-1 blocked migration. This report provides the first evidence that B cell precursors exhibit chemotactic responses to a specific chemokine.
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D'Apuzzo, M.1
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0031571743
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Primary B cell development is impaired in mice with defects of the pituitary/thyroid axis
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0031158981
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40
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0030875168
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Increased B-lymphopoiesis by interleukin 7 induces bone loss in mice with intact ovarian function: Similarity to estrogen deficiency
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+ B-cells in BM. Furthermore, IL-7 administration enhanced B-cell lymphopoiesis and stimulated bone loss in female mice. Mice deficient in IL-7-receptor exhibited increased trabecular bone volume compared with wild-type littermates. These results identify a previously unrecognized relationship between bone metabolism and lymphopoiesis
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+ B-cells in BM. Furthermore, IL-7 administration enhanced B-cell lymphopoiesis and stimulated bone loss in female mice. Mice deficient in IL-7-receptor exhibited increased trabecular bone volume compared with wild-type littermates. These results identify a previously unrecognized relationship between bone metabolism and lymphopoiesis. B cell precursors or IL-7 could directly or indirectly promote osteoclast activation and bone resorption. It is noteworthy that lymphoid cells can stimulate BM stromal cells to produce IL-6 [25], a potential mediator of bone resorption.
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Miyaura, C.1
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41
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0031156933
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Apoptosis during B lymphopoiesis in mouse bone marrow
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- cells. These data are consistent with loss of B-lineage cells via activation of apoptotic pathways in cells that have made nonfunctional H chain rearrangements, and immature B cells undergoing negative selection. A provisional model was presented that included estimates of daily B-lineage cell production and loss (through apoptosis) in vivo, as a function of the stage of B cell development.
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- cells. These data are consistent with loss of B-lineage cells via activation of apoptotic pathways in cells that have made nonfunctional H chain rearrangements, and immature B cells undergoing negative selection. A provisional model was presented that included estimates of daily B-lineage cell production and loss (through apoptosis) in vivo, as a function of the stage of B cell development.
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Lu, L.1
Osmond, D.G.2
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42
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0031279146
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Stromal cell modulation of negative regulatory signals that influence apoptosis and proliferation of B lineage lymphocytes
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of special interest. The objective of this study was to analyze murine stromal cell lines established from various hematopoietic tissues for their capacity to inhibit apoptosis of B cell precursors. Most stromal cells inhibited apoptosis through a mechanism dependent on contact, but not on vascular cell adhesion molecule-1, although one bone marrow (BM) stromal cell line appeared to enhance apoptosis. Lymphoid cell apoptosis induced by glucocorticoids and cytokines (e.g. IL-1α) was reduced by stromal cell contact. These results support the hypothesis that interactions between multiple lymphoid cells and stromal cell receptors and ligands probably mediate apoptosis (through activation or inhibition) in the BM microenvironment.
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of special interest Borghesi LA, Smithson G, Kincade PW. Stromal cell modulation of negative regulatory signals that influence apoptosis and proliferation of B lineage lymphocytes. J Immunol. 159:1997;4171-4179 The objective of this study was to analyze murine stromal cell lines established from various hematopoietic tissues for their capacity to inhibit apoptosis of B cell precursors. Most stromal cells inhibited apoptosis through a mechanism dependent on contact, but not on vascular cell adhesion molecule-1, although one bone marrow (BM) stromal cell line appeared to enhance apoptosis. Lymphoid cell apoptosis induced by glucocorticoids and cytokines (e.g. IL-1α) was reduced by stromal cell contact. These results support the hypothesis that interactions between multiple lymphoid cells and stromal cell receptors and ligands probably mediate apoptosis (through activation or inhibition) in the BM microenvironment.
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Borghesi, L.A.1
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43
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44
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0029958003
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46
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0030873513
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Contact between human bone marrow stromal cells and B lymphocytes enhances very late antigen-4/vascular cell adhesion molecule-1-independent phosphorylation of focal adhesion kinase, paxillin, and ERK2 in stromal cells
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of special interest. This study is an extension of a prior report [25] demonstrating that human VLA-4-deficient lymphoid cells can induce tyrosine kinase activation and IL-6 production by human bone marrow (BM) stromal cells. An experimental strategy was developed that facilitates the detection of specific tyrosine-phosphorylated substrates in stromal cells 'stimulated' by lymphoid cell contact. Lymphoid cell contact induced tyrosine phosphorylation of focal adhesion kinase and paxillin in normal BM stromal cells within five minutes, a time period less than that usually required to achieve a steady-state adhesive interaction between these two cell types
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of special interest Jarvis LJ, Maguire JE, LeBien TW. Contact between human bone marrow stromal cells and B lymphocytes enhances very late antigen-4/vascular cell adhesion molecule-1-independent phosphorylation of focal adhesion kinase, paxillin, and ERK2 in stromal cells. Blood. 90:1997;1626-1635 This study is an extension of a prior report [25] demonstrating that human VLA-4-deficient lymphoid cells can induce tyrosine kinase activation and IL-6 production by human bone marrow (BM) stromal cells. An experimental strategy was developed that facilitates the detection of specific tyrosine-phosphorylated substrates in stromal cells 'stimulated' by lymphoid cell contact. Lymphoid cell contact induced tyrosine phosphorylation of focal adhesion kinase and paxillin in normal BM stromal cells within five minutes, a time period less than that usually required to achieve a steady-state adhesive interaction between these two cell types. Lymphoid cell contact also induced the tyrosine phosphorylation of ERK2 and the ERK2 substrate Elk1 (a transcription factor). This report demonstrates the feasibility of studying the activation of signaling pathways dependent on tyrosine kinases in stromal cells, and should facilitate a more detailed exploration of the biochemical changes that occur in the nonhematopoietic component of the BM.
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Jarvis, L.J.1
Maguire, J.E.2
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47
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48
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0030483542
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Identification of the earliest B lineage stage in mouse bone marrow
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+) cells
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+) expressed germline μ, RAG-1, RAG-2, Igα, Igβ and λ5 gene transcripts. This refinement of the earliest stages of B cell development provides potential opportunities for investigating whether cytokines or stromal cell membrane-associated molecules can activate transcription of germline μ. RAG-1, RAG-2 and Ig-β genes.
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50
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51
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0029793903
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Abnormal B cell development activation, and differentiation in mice that lack or overexpress the CD19 signal transduction molecule
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0031253851
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Regulation of B lymphocyte development and activation by the CD19/CD21/CD81/Leu 13 complex requires the cytoplasmic domain of CD19
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59
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0031183025
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CD38 ligation in human B cell progenitors triggers tyrosine phosphorylation of CD19 and association of CD19 with lyn and phosphatidylinositol 3-kinase
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60
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0031307605
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Differential induction of DNA-binding activities following CD19 cross-linking in human B-lineage cells
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Weng W-K1
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61
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0030840883
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H gene segment transcription and rearrangement before surface expression of the pan-B-cell marker CD19 in normal human bone marrow
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+ pro-B cells. These results convincingly show that CD19 surface expression occurs subsequent to the initial stages of immunoglobulin gene rearrangement/expression. Hence, CD19 expression is probably an indication or manifestation of B-lineage commitment, rather than a mediator of commitment.
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+ pro-B cells. These results convincingly show that CD19 surface expression occurs subsequent to the initial stages of immunoglobulin gene rearrangement/expression. Hence, CD19 expression is probably an indication or manifestation of B-lineage commitment, rather than a mediator of commitment.
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Blood
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Bertrand, F.E.1
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Burrows, P.D.3
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62
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0030892090
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Expression of interleukin-7 receptor by lineage-negative human bone marrow progenitors with enhanced lymphoid proliferative potential and B-lineage differentiation capacity
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- cells had greatly reduced clonogenic capacity and failed to differentiate into pro-B cells. These results suggest a potential role
-
+ cells in this culture system.
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-
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Ryan, D.H.1
Nuccie, B.L.2
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Davi, F.1
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64
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0030442576
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Ordering of human bone marrow B lymphocyte precursors by single-cell polymerase chain reaction analyses of the rearrangement status of the immunoglobulin H and L chain gene loci
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- cells. Ghia and colleagues quite convincingly
-
+ populations into a developmental hierarchy will necessitate purification of cells by fluorescence-activated cell sorters and in vitro assays that support differentiation of the three pre-B populations.
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Ghia, P.1
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67
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Marshall, A.J.1
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