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Blockade of the CD28 costimulatory pathway: A means to induce tolerance
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Boussiotis VA, Gribben JG, Freeman GJ, Nadler LM: Blockade of the CD28 costimulatory pathway: a means to induce tolerance. Curr Opin Immunol 1994, 6:797-807.
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Lenschow DJ, Walunas TL, Bluestone JA: CD28/B7 system of T cell costimulation. Annu Rev Immunol 1996, 14:233-258. This is a comprehensive review that summarizes the in vitro and in vivo studies that have led to our current understanding of the B7-CD28/CTLA 4 pathway and its regulatory role in the immune response.
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CTLA-4 can function as a negative regulator of T cell activation
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Walunas TL, Lenschow DJ, Bakker CY, Linsley PS, Freeman GJ, Green JM. Thompson CA, Bluestone JA: CTLA-4 can function as a negative regulator of T cell activation. Immunity 1994, 1:405-413.
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Walunas, T.L.1
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6
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0000067011
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CTLA-4 mediated costimulation induces apoptosis of activated human T lymphocytes
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Gribben JG, Freeman GJ, Boussiotis VA, Rennert P, Jellis CL, Greenfield E, Barber M, Gray GS, Nadler LM: CTLA-4 mediated costimulation induces apoptosis of activated human T lymphocytes. Proc Natl Acad Sci USA 1994, 92:811-815.
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Gribben, J.G.1
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Greenfield, E.6
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0029120245
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CD2B and CTLA-4 have opposing effects on the response of T celts to stimulation
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Krummel M, Allison J: CD2B and CTLA-4 have opposing effects on the response of T celts to stimulation. J Exp Med 1995, 182:459-466. Similar to [5,6], this study also suggests that CTLA-4 delivers an inhibitory signal to the T cell. T cells did not proliferate when stimulated with an antiCTLA-4 mAb and a suboptimal concentration of anti-CD3. In contrast, blocking CTLA-4 engagement with soluble anti-CTLA-4 mAbs enhanced the proliferation of T cells stimulated with anti-CD3 and anti-CD28 In the presence of cross-linking antibodies, however, anti-CTLA-4 inhibited proliferation of T cells and IL-2 production by T cells incubated with anti-CD3 and anti-CD28.
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Krummel, M.1
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8
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0028867420
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Loss of CTLA-4 leads to massive lymphoproliferation and fatal multiorgan tissue destruction, revealing a critical negative regulatory role of CTLA-4
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Tivol EA, Borriello F, Schweitzer AN, Lynch WP, Bljestone JA, Sharpe AH: Loss of CTLA-4 leads to massive lymphoproliferation and fatal multiorgan tissue destruction, revealing a critical negative regulatory role of CTLA-4. Immunity 1995. 3:541-547. This paper describes the phenotype of CTLA-4-deficient mice, which revealed a critical role for CTLA-4 in downregulating T cell activation. The mice suffered lymphadenopathy and splenomegaly, developed particularly severe myocarditis and pancreatitis, and died at 3-4 weeks of age, The T cells of these mice proliferated spontaneously in vitro and produced abundant cytokines See also [9**].
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Immunity
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Tivol, E.A.1
Borriello, F.2
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Sharpe, A.H.6
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9
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Lymphoproliferative disorders with early lethality in mice deficient in CTLA-4
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-/- T cells remain sensitive to cell death induced by either cross-linking of the FasR or gamma irradiation.
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Waterhouse, P.1
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0030113898
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Lymphocyte activation: T cell regulation . by CTLA-4
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Linsley PS, Golstein P: Lymphocyte activation: T cell regulation . by CTLA-4. Gun Biol 1996, 4:398-400. This is a concise, thoughtful review comparing the functions of CTLA-4 and CD28.
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Gun Biol
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Linsley, P.S.1
Golstein, P.2
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11
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0030176371
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Intracellular trafficking of CTLA-4 and focal localization towards sites of TCR engagement
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Linsley PS, Bradshaw J. Greene J, Peach R, Bennett KL, Mittler RS: Intracellular trafficking of CTLA-4 and focal localization towards sites of TCR engagement Immunity 1996, 4:535-544.
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Linsley, P.S.1
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12
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0028675006
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Human B7-1 (CD80) and B7-2 (CD86) bind with similar avidities but distinct kinetics to CD28 and CTLA4 receptors
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2. Linsley PS, Greene JL, Brady W, Bayorath J, Ledbetter JA, Peach R: Human B7-1 (CD80) and B7-2 (CD86) bind with similar avidities but distinct kinetics to CD28 and CTLA4 receptors. Immunity 1994, 1:793-801.
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Linsley, P.S.1
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13
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Differential up-regulation of the B7-1 and B7-2 costimulatory molecules following immunoglobulin receptor engagement by antigen
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Lenschow DJ, Sperling AI, Cooke MP, Freeman G, Rhee L, Decker DC, Gray G, Nadler LM, Goodnow CC, Bluestone JA: Differential up-regulation of the B7-1 and B7-2 costimulatory molecules following immunoglobulin receptor engagement by antigen. J Immunol 1994, 153:1990-1997.
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Lenschow, D.J.1
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14
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0029073050
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B7-1 and B7-2 do not deliver identical costimulatory signals, since B7-2 but not B7-1 preferentially costimulates the initial production of IL-4
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Freeman GJ, Boussiotis VA, Anumanthan A, Bernstein GM, Ke X-Y, Rennert PD, Gray GS, Gribben JG, Nadler LM: B7-1 and B7-2 do not deliver identical costimulatory signals, since B7-2 but not B7-1 preferentially costimulates the initial production of IL-4. Immunity 1995, 2:523-532. These studies compared the function of B7-1 and B7-2 in vitro using Chinese hamster ovary cell transfectants expressing either human B7-1 or B7-2. These transtactants equivalently costimulated human CD4+ T cells to produce IL-2 and interferon-γ. B7-2 transfectants induced significantly more IL-4 production than B7-1, however, with the greatest difference seen in naive T cells. These studies suggest a preferential role for B7-2 in Th2 Subset differentiation.
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Immunity
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Freeman, G.J.1
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Nadler, L.M.9
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15
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0030026868
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B7-1 but not B7-2 efficiently costimulates CD8+ T lymphocytes in the PB15 tumor system in vitro
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Gajewski TF: B7-1 but not B7-2 efficiently costimulates CD8+ T lymphocytes in the PB15 tumor system in vitro. J Immunol 1996. 156:465-472
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Gajewski, T.F.1
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16
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0028819315
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CD8D (B7) and CD8G (B70) provide similar costimulatory signals for T cell proliferation, cytoktne production, and generation of CTL
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Lanier LL, O'Fallon S, Somoza C, Phillips JH, Linsley, PS, Okumara K, Ito D, Azuma M: CD8D (B7) and CD8G (B70) provide similar costimulatory signals for T cell proliferation, cytoktne production, and generation of CTL. J Immunol 1995, 154:97-105.
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Lanier, L.L.1
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Ito, D.7
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17
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0026486220
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Coexpression and functional cooperation of CTLA-4 and CD28 on activated T lymphocytes
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Linsley PS, Greene JL, Tan P, Bradshaw J, Ledbetter JA, Anasetti C, Damle NK: Coexpression and functional cooperation of CTLA-4 and CD28 on activated T lymphocytes. J Exp Med 1992, 176:1595-1604.
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Linsley, P.S.1
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Damle, N.K.7
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19
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0029960141
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Superantigen responses and costimulation: CD28 and CTLA-4 have opposing effects on T cell expansion in vitro and in vivo
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Krummel MF, Sullivan TJ, Allison JP: Superantigen responses and costimulation: CD28 and CTLA-4 have opposing effects on T cell expansion in vitro and in vivo. Int Immunol 1995, 8:519-523.
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Int Immunol
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Krummel, M.F.1
Sullivan, T.J.2
Allison, J.P.3
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20
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0029986723
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Evidence that induction of tolerance in vivo involves active signaling via a B7 liganddependent mechanism: CTLA4-lg protects Vβ8+ T cells from tolerance induction by the superantfgen staphylococcal enterotoxin B
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+ T cells from CTLA-4-lg transgenic mice were not anergic and remained responsive to superantigen in vitro. Therefore, CTLA-4-lg was found to prevent, rather than facilitate, tolerance induction in CD4+ T cells. This study suggests that signaling via a B7-dependent mechanism is needed to induce tolerance.
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(1996)
Eur J Immunol
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, pp. 358-862
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Lane, P.1
Haller, C.2
McConnell, F.3
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21
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0028670596
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Apoptosis, Fas, and systemic autoimmunity: The MRL-lpr/lpr model
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Singer GG, Carrera AC, Marshak-Rothstein A, Martinez A-C, Abbas AK: Apoptosis, Fas, and systemic autoimmunity: the MRL-lpr/lpr model. Cure Opin Immunol 1994, 6:913-920.
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Singer, G.G.1
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Abbas, A.K.5
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22
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0030175603
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Role of Fas-mediated cell death in the regulation of immune responses
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Van Parijs L, Abbas AK: Role of Fas-mediated cell death in the regulation of immune responses. Curr Opin Immunol 1996, 8:355-331. A recent thoughtful review of the role of the Fas-FasL pathway in salf-tolerance and autoimmunity. The recent advances in the biochemical mechanisms of Fas-mediated killing are summarized.
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Curr Opin Immunol
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Van Parijs, L.1
Abbas, A.K.2
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23
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0029947568
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Enhancement of antitumor immunity by CTLA-4 blockade
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Leach DR, Krummel MF, Allison JP: Enhancement of antitumor immunity by CTLA-4 blockade. Science 1996, 271:1734-1 736. This study demonstrates thai anti-CTLA-4 mAbs can accelerate the rejection of both B7-1 positive and B7-1 negative colon carcinoma cells, and can protect against subsequent carcinoma cell challenge. Anti-CTLA-4 treatment also reduced the growth of established tumors, suggesting that blocking the inhibitory effects of CTLA-4 can enhance antitumor immune responses at both early and later stages of tumor development.
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(1996)
Science
, vol.271
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Leach, D.R.1
Krummel, M.F.2
Allison, J.P.3
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24
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0029789389
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CTLA-4: A negative regulator of autoimmune disease
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Karandikar N, Vanderlugt CL, Walunas TL, Miller SD, Bluastone JA: CTLA-4: a negative regulator of autoimmune disease. J Exp Mad 1996, 134:783-788. This study explores the role of CTLA-4 in the development of EAE. Treatment of T cell clones specific for PLP139-151 with anti-CTLA-4 mAbs enhanced both their proliferation in vitro and their ability to induce disease in vivo. AntiCTLA-4 mAb treatment of recipients of adoptively-transferred activated PLPspecific T cells accelerated and exacerbated disease. Anti-CTLA-4 treatment of mice also exacerbated relapses in R-EAE. These observations suggest that CTLA-4 plays a significant role in the development of EAE. (See also [25-].)
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J Exp Mad
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Karandikar, N.1
Vanderlugt, C.L.2
Walunas, T.L.3
Miller, S.D.4
Bluastone, J.A.5
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25
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0030586626
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CTLA-4 blockade enhances clinical disease and cytokine production during experimental allergic encephalomyelitis
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Perrin R Maldonado J, Davis TA, June CH, Racke MK: CTLA-4 blockade enhances clinical disease and cytokine production during experimental allergic encephalomyelitis. J Immunol 1996, 157:1333-1336. Similar to [24*], this study shows that anti-CTLA-4 mAb treatment can exacerbate EAE. Treatment with anti-CTLA-4 after the onset of clinical symptoms increased disease severity and proinflammatory cytokine production,
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J Immunol
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Maldonado J, P.R.1
Davis, T.A.2
June, C.H.3
Racke, M.K.4
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26
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0029899783
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CTLA-4 engagement inhibits IL-2 accumulation and cell cycle progression upon activation of resting T cells
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Krummel MF, Allison JP: CTLA-4 engagement inhibits IL-2 accumulation and cell cycle progression upon activation of resting T cells. J Btp Med 1996, 183:2533-2540. This study examines the events following CTLA-4 engagement in freshly isolated CD3+ T cells. Ligation of CTLA-4 inhibited proliferation and IL-2 production in cells stimulated with immobilized anti-CD3 and anti-CD28, but had no effect on viability or the induction of apoptosis. Inhibition of proliferation appears to be a consequence of arrest of cells in G.yG, stage of the cell cycle, possibly due to diminished IL-2 production. CTLA-4 engagement also inhibited the expression of IL-2R and CD69, indicating that CTLA-4 signaling inhibits an early stage of T cell activation. (See also 127'].)
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J Btp Med
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Krummel, M.F.1
Allison, J.P.2
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27
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0029953858
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CTLA-4 ligation blacks CD28-dependent T cell activation
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Walunas TL, Bakker CY, Bljestone JA: CTLA-4 ligation blacks CD28-dependent T cell activation. J Exp Med 1993, 183:2541-2550. Similar to (26*), this study investigates the mechanism by which CTLA-4 blocks CO28-mediated activation of T cells. Incubation of activated CD3+ lymph node cells with anti-CTLA-4 antibodies inhibited proliferation, IL-2 production, IL-2R expression, and cell cycle progression, but did not induce apoptosis. The addition of exogenous IL-2 restored proliferation and IL-2R expression, suggesting that CTLA-4 signaling blocks CD28-mediated activation by inhibiting IL-2 production. It should be noted that the anti-CTLA-4 mAbs used in this study and in (26') could block B7-CTLA-4 interactions, in contrast to the mAbs used in [6], which bound to a distinct epitope and could induce apoptosis.
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J Exp Med
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Walunas, T.L.1
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28
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0030001318
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Regulation of T cell receptor signaling by tyrosine phosphatase syp association with CTLA-4
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Marengere LEM, Waterhouse P, Duncan GO, Mittrucker H, Feng G, Mak TW: Regulation of T cell receptor signaling by tyrosine phosphatase syp association with CTLA-4. Science 1996, 272:1170-1173, This study shows that the Ras pathway and the TCR-specific kinases Fyn, Lck, and ZAP-70 are hyperactivated in CTLA-4- T cells. Targets of tyrosine phosphorylation after TOR activation, including CDSt, and p52Sh(: were hyperphosphorylated in CTLA-4- T cells. An association of CTLA-4 with the tyrosine phosphatase, SYP, was demonstrated, suggesting that CTLA-4 regulates CD28-mediated activation of tyrosine kinases through SYP.
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Science
, vol.272
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Marengere, L.E.M.1
Waterhouse, P.2
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Mak, T.W.6
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29
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0029012969
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A role in B cell activation for CD22 and the protein tyrosine phosphatase SHP
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Doody GM, Justement LB, Delibrias CC, Matthews RJ, Lin J, Thomas ML, Fearon DT: A role in B cell activation for CD22 and the protein tyrosine phosphatase SHP. Science 1995, 269:242-244.
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Science
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Doody, G.M.1
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30
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0030047811
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CD22 associates with protein tyrosine phosphatase 1C, syk, and phospholipase C-gamma upon B cell activation
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Law CL, Sidarenko SP, Chandran KA, Zhao Z, Shen SH, Fischer EH, Clark EA: CD22 associates with protein tyrosine phosphatase 1C, syk, and phospholipase C-gamma upon B cell activation. J Exp Wed 1996. 183:547-560
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J Exp Wed
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Law, C.L.1
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Fischer, E.H.6
Clark, E.A.7
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31
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0028997875
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Of ITAMS and ITIMS: Turning on and off the B cell antigen receptor
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Thomas ML: Of ITAMS and ITIMS: turning on and off the B cell antigen receptor. J Exp Wed 1995, 181:1953-1955.
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Thomas, M.L.1
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0030024788
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Recruitment of tyrosine phosphatase HCP by the killer cell inhibitor receptor
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Burshtyn DM, Scharenberg AM, Wagtmann M, Rajagopalan S, Berrada K, Yi T, Kinet JP, Long EO: Recruitment of tyrosine phosphatase HCP by the killer cell inhibitor receptor. Immunity 1996, 4:77-85.
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Immunity
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Burshtyn, D.M.1
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Yi, T.6
Kinet, J.P.7
Long, E.O.8
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33
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0028921849
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Potential roles of the B7 and CD28 receptor families in autoimmunity and immune evasion
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Harlan DM, Abe R, Lee KP, June CH: Potential roles of the B7 and CD28 receptor families in autoimmunity and immune evasion. Clin Immunol Imrnuncpathol 1995, 75:99-111. This is a thoughtful analytical review of the B7-CD28/CTLA-4 pathway, which emphasizes the clinical potential of manipulating this pathway for immunosuppression or immunostimulation.
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(1995)
Clin Immunol Imrnuncpathol
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Harlan, D.M.1
Abe, R.2
Lee, K.P.3
June, C.H.4
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34
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0028999041
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Long-term inhibition of murine experimental autoimmune encephalomyelitis using CTLA4-Fc supports a key role lor CD2B stimulation. 1
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Cross AH, Girard TJ, Giacoletto KS, Evans RJ, Keeling RM, Lin RF, Trotter JL, Karr RW: Long-term inhibition of murine experimental autoimmune encephalomyelitis using CTLA4-Fc supports a key role lor CD2B (stimulation. 1 Clin Invest 1995, 95:2783-2789. This study shows that CTLA-4-Ig can prevent the induction of EAE and lead to effective long-term suppression of EAE, even altar the cessation of treatment. T cells from these mica could still proliferate in response to PLP in vitro and could transfer EAE upon adoptive transfer, however, suggesting that CTLA-4-lg treatment did not induce T cell tolerance to antigen. This study demonstrates an important role for B7-CD28/CTLA-4 interactions in the pathogenesis of EAE and suggests the clinical potential for this therapeutic approach for MS.
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(1995)
Clin Invest
, vol.95
, pp. 2783-2789
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Cross, A.H.1
Girard, T.J.2
Giacoletto, K.S.3
Evans, R.J.4
Keeling, R.M.5
Lin, R.F.6
Trotter, J.L.7
Karr, R.W.8
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35
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0028785417
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Distinct roles for B7-1 (CD80) and B7-2 (CD86) in the initiation of experimental allergic encephalomyelitis
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Racke MK, Scott DE, Quigley L, Gray GS, Abe R, June CH, Perrin PJ: Distinct roles for B7-1 (CD80) and B7-2 (CD86) in the initiation of experimental allergic encephalomyelitis. J Clin Invest 1995, 96:2195-2203. This study examines the effects of manipulation of the B7-CD29/CTLA-4 pathway in the active and passive transfer models of EAE. In actively induced EAE, a single injection of anti-B7-1 could significantly reduce disease, whereas anti-B7-2 exacerbated disease. A single injection of CTLA-4-lg two days after immunization could suppress disease, whereas multiple injections ol CTLA-4-lg (from day -1 to day 1 7) could enhance disease. In adoptively transferred EAE, in vitro activation of MBP-specific T cells could be markedly inhibited by anti-87-1 plus anti-B7-2, but by neither mAb individually. This in vitro treatment with anti-B7-1 and B7-2 led to a delay in the onset and a reduction in the severity of clinical disease upon the adoptive transfer of the treated MBP-specific T cells. This study illustrates the potential promise, as well as the difficulties, in manipulating this pathway lor therapeutic benefits. The timing of treatment appears critical, and may be related to the distinct temporal expression of the receptors and ligands in the pathway and their complex interactions, which can result in positive or negative signals for T cell activation.
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(1995)
J Clin Invest
, vol.96
, pp. 2195-2203
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Racke, M.K.1
Scott, D.E.2
Quigley, L.3
Gray, G.S.4
Abe, R.5
June, C.H.6
Perrin, P.J.7
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36
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0028814279
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Role of B7/CD28 CTLA-4 in the induction of chronic relapsing experimental allergic encephalomyelitis
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Perrin PJ, Scott D, Quigley L, Albert PS, Feder O, Gray GS, Abe R, June CH, Racke MK: Role of B7/CD28 CTLA-4 in the induction of chronic relapsing experimental allergic encephalomyelitis. J Immunol 1995, 154:1481-1490. This study examines the effects of CTLA-4-lg administration at various times during chronic R-EAE induced by the transfer of MBP specific T cell lines. CTLA-4-lg treatment o( MBP-primed lymph node cells in vitro prior to transfer attenuated the induction of R-EAE. When CTLA-4-lg was administered to donor mice (from day -1 lo day 10) immunized with MBP and the primed cells were incubated with CTLA-4-lg prior to transfer, there was a marked Suppression of R-EAE. CTLA-4-lg treatment of recipients of activated MBPspecrfic T cells neither affected disease course nor severity, however. These data suggest that the B7-CD28/CTLA-4 pathway plays an important role in the development of encephalitogenic T cells and in the establishment of R-EAE.
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J Immunol
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Perrin, P.J.1
Scott, D.2
Quigley, L.3
Albert, P.S.4
Feder, O.5
Gray, G.S.6
Abe, R.7
June, C.H.8
Racke, M.K.9
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37
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0028868424
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CD28-B7 costimulatory blockade by CTLA4lg prevents actively induced experimental autoimmune encephalomyelitis and inhibits Th1 but spare Th2 cytokines in the central nervous System
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Khoiiry SJ, Akalin E, Chandraker A, Turka LA, Linsley PS, Sayegh MH, Hancock WW. CD28-B7 costimulatory blockade by CTLA4lg prevents actively induced experimental autoimmune encephalomyelitis and inhibits Th1 but spare Th2 cytokines in the central nervous System. J Immunol 1995, 155:4521-4524. This study examines the effects of CTLA-4-lg on the course of EAE in the Lewis rat model. CTLA-4-lg administered from day 0 to day 10 significantly reduced the incidence, duration, and severity of EAE. When CTLA-4-lg treatment was begun on day 7 or day 10 after immunization when pathological disease was present, there was still a marked suppression of disease. The CTLA-4-lg protective effect could not be reversed by in vivo administration of IL-2. Immunohistological analyses of rats treated with CTLA-4-lg indicated thai CTLA-4-lg inhibited trie inflammatory Th1 response in the CNS, and upregulated protective Th2 cytokines, suggesting that CTLA-4-lg mediates protective effects by immune deviation. See also [38*].
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J Immunol
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Khoiiry, S.J.1
Akalin, E.2
Chandraker, A.3
Turka, L.A.4
Linsley, P.S.5
Sayegh, M.H.6
Hancock, W.W.7
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38
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0029886610
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Inhibition by CTLA-4-Ig of experimental allergic encephalomyelitis. 1
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Arima T, Rehman A, Mickey WF, Flye MW: Inhibition by CTLA-4-Ig of experimental allergic encephalomyelitis. 1 Immunol 1996, 156:4916-4924. Similar to [37*], this study examines the effects of CTLA-4-lg on the course of EAE in the Lewis rat model. CTLA-4-lg treatment from days -2 to +18 markedly decreased the incidence and severity of EAE. In contrast to (37*], when CTLA-4-lg treatment was begun on day 7 postimmunization, there was no CTLA-4-lg protective effect observed. In addition, IL-2 abrogated the protective effect of CTLA-4-lg in this study, in contrast to [37-]. Whether the differences could relate to the timing of CTLA-4-lg administration or to the dose of IL-2 administered is not clear.
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Immunol
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Arima, T.1
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39
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Differential effects of anti-B7-1 and antiB7-2 monoclonal antibody treatment on the development of diabetes in the nonobese diabetic mouse
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Lenschow DJ, Ho SC, Sattar H, Rhee L, Gray G, Nabavi N, Herold KC, Bluestone JA: Differential effects of anti-B7-1 and antiB7-2 monoclonal antibody treatment on the development of diabetes in the nonobese diabetic mouse. J Exp Med 1995, 181:1145-1155. Early administration of murine CTLA-4-lg to female NOD mice inhibits the development of diabetes, but not insulitis. Late administration of CTLA-4-lg, however, is of no benefit. Blocking signaling via B7-2 also inhibits disease, although treatment with anti-B7-1 results in increased frequency of disease in males and accelerated disease in females. These data suggest that B7-1 and B7-2 play different roles in the development of type I diabetes.
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(1995)
J Exp Med
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Lenschow, D.J.1
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Herold, K.C.7
Bluestone, J.A.8
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40
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0028483990
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Treatment of murine lupus with CTLA4lg
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Finck B, Linsley P Wofsy D: Treatment of murine lupus with CTLA4lg. Science 1994, 265:1225-1227.
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Finck, B.1
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41
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0028949152
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B7-1 and B7-2 costimulatory molecules differentially activate the Th1/Th2 developmental pathways: Application to autoimmune disease therapy
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Kuchroo V, Prabhu Das M, Brown JA, Ranger AM, Zanwil SS, Sobel RA, Weiner HL, Nabavi N, Glimcher LH: B7-1 and B7-2 costimulatory molecules differentially activate the Th1/Th2 developmental pathways: application to autoimmune disease therapy. Cell 1995, 80:707-716. This study snows that anti-B7-1 mAbs administered at the time of immunization with PLP139-151 can reduce the incidence of acute EAE, whereas antiB7-2 mAbs increased disease severity. Anti-B7-1 mAbs did not inhibit the induction of PLP-specific T cells, but instead altered the cytokine profile of the responding cells, resulting in the predominant generation of Th2 clones, whose transfer both prevented induction of EAE and abrogated established disease. This study suggests that anti-B7-1 can block Thl activation and consequently the progression of EAE. The data show that manipulation of the B7-CD28/CTLA-4 pathway can skew the balance of the immune response by influencing the nature of the cytokines produced in response to antigen exposure.
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(1995)
Cell
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Kuchroo, V.1
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Weiner, H.L.7
Nabavi, N.8
Glimcher, L.H.9
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42
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0029553431
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Blockade of CD2B/B7-1 interaction prevents epitope spreading and clinical relapses of murine EAE
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Miller SD, Vanderlugt CL, Lenschow DJ, Pope JG, Karandikar NJ, Dal Canto MC, Bluestone JA: Blockade of CD2B/B7-1 interaction prevents epitope spreading and clinical relapses of murine EAE. immunity 1 995, 3:739-745. This study examined the expression of B7-1 and B7-2 during the course of R-EAE and found that B7-1 is preferentially upregulated When mice were treated with anti-B7-1 Fab fragments after recovery from the acute paralytic disease, both clinical relapses and epitope spreading were prevented. This study points to a critical role for B7-1 in the perpetuation of the chronic stages of inflammatory autoimmune disease.
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(1995)
Immunity
, vol.3
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Miller, S.D.1
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Dal Canto, M.C.6
Bluestone, J.A.7
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43
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0028834366
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Preferential dependence of autoantibody production in murine lupus on CD86 costimulatory molecule
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2a. Treatment with both mAbs after trie onset of lupus led to prolonged survival with reduced autoantibody production. These data suggest that blockade of both B7 ligands is needed to prevent the development and progression of lupus, but that B7-2 plays a more critical role than B7-1 in autoantibody production and contributes to Th2-mediated IgG production.
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(1995)
Eut J Immunol
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Nakajima, A.1
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Hirose, S.7
Shirai, T.8
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44
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0029558631
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Pancreatic expression of B7 costimulatory molecules in the non-obese diabetic mouse
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Stephens L, Kay I: Pancreatic expression of B7 costimulatory molecules in the non-obese diabetic mouse. Int Immunol 1995, 7:1865-1665.
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Int Immunol
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Stephens, L.1
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45
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0028824684
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Signal transduction by B7/BB1 expressed on activated T lymphocytes-crosslinking of B7/BB1 induces protein tyrosine phosphorylation and synergizes with signalling through T-cell receptor/CD3
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Hirokawa M, Kitabayashi A, Kuroki J, Miura AB: Signal transduction by B7/BB1 expressed on activated T lymphocytes-crosslinking of B7/BB1 induces protein tyrosine phosphorylation and synergizes with signalling through T-cell receptor/CD3. Immunology 1995, 86:155-161.
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Hirokawa, M.1
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46
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0028809507
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Expression of costimulatory molecules B7-1 (CD80), B7-2 (CD86) and Interleukin 12 cytoklne in multiple sclerosis lesions
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Windhagen A. Newcornbe J, Dangond F, Strand C, Woodroofe MM, Cuzner ML, Hafler DA: Expression of costimulatory molecules B7-1 (CD80), B7-2 (CD86) and Interleukin 12 cytoklne In multiple sclerosis lesions. J Exp Med 1995, 182:1985-1996, This study compared B7-1 and B7-2 expression In CNS tissue from patients with MS, chronic virus-induced inflammatory lesions, inflammatory infarcts, and patients without any known CNS pathology. B7-1 and IL-12 p40 expression were observed in acute MS plaques, but not in inflammatory infarcts or control brain tissue. B7-1 staining was localized primarily to lymphocytes in perivascular inflammatory cuffs. B7-2 was expressed primarily on macrophages both in MS plaques and in inflammatory infarcts. These results suggest that an early event in the initiation of MS leads to upregulation of B7-1 and IL-12, enhancing T cell activation.
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J Exp Med
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Windhagen, A.1
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Woodroofe, M.M.5
Cuzner, M.L.6
Hafler, D.A.7
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47
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0028964455
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The costimulatory molecule B7 is expressed on human microglia in culture and in multiple sclerosis acute lesions
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De Simone R, Giampaolo A, Giometto B, Gallo R Levi G, Peschle C, Aloisi F: The costimulatory molecule B7 is expressed on human microglia in culture and in multiple sclerosis acute lesions. J Neuropathol Erp Neural 1995, 54:175-187.
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48
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B7/BB1 antigen expression on adult human microglia studied in vitro and in situ
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49
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0027996295
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Elevated expression of CD80 (BA/8B1) and other accessory molecules on synovial fluid mononuclear cell subsets in rheumatoid arthritis
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Ranheim EA, Kipps TJ : Elevated expression of CD80 (BA/8B1) and other accessory molecules on synovial fluid mononuclear cell subsets in rheumatoid arthritis. Arthritis Rheum 1994, 37:1637-1646.
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Ranheim, E.A.1
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50
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0028244233
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Expression of functional B7 and CTLA4 on rheumatoid synovial T cells
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Verwilghen J, Lovis R, De Boer M, Linsley P, Haines G, Koch A, Pope R: Expression of functional B7 and CTLA4 on rheumatoid synovial T cells. J Immunol 1994, 153:1378-1365,
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51
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Expression of the costimulatory molecule B7/BB1 antigen in autoimmune thyroid disease
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Tandon N, Uetcalfe R, Barren D, Weetman A: Expression of the costimulatory molecule B7/BB1 antigen in autoimmune thyroid disease. Quart J Med 1994, 87:231-236.
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53
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T lymphocytes in skin lesions of psoriasis and mycosis fungoides express B7-1 : A ligand for CD28
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Nickoloff B, Nestle F. Zheng X, Turks L: T lymphocytes in skin lesions of psoriasis and mycosis fungoides express B7-1 : a ligand for CD28. Blood 1994, 83:2560-2536.
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Analysis of lymphocyte costimulation in vivo using transgenic and 'knockout' mice
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S harpe AH: Analysis of lymphocyte costimulation in vivo using transgenic and 'knockout' mice. Curr Opin Immunol 1995, 7:389-395. This article focuses or the furctional evaluation of costimulatary pathways using transgenic approaches and discusses insights obtained from the analyses of mice lacking or overexpressing costimulatory molecules.
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Sharpe, A.H.1
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Costimulator B71 confers antigen-presenting-cell function to parenchyma I tissue and in conjunction with tumor necrosis factor a leads to autoimmunity in transgenic mice
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Guarder S, Picarella DE, Linsley P, Flavell RA: Costimulator B71 confers antigen-presenting-cell function to parenchyma I tissue and in conjunction with tumor necrosis factor a leads to autoimmunity in transgenic mice. Proc Natl Acad Sci USA 1994, 91:5138-5142.
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56
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Characterization of the murine B7-1 genomic locus reveals an additional exon encoding an alternative cytoplasmic domain and a chromosomal location to chromosome 16, band 5
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57
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The gene for B7, a costimulatory signal for T cell activation, maps to chromosomal region 3q13.3-3q21
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Freeman GJ, Disteche CM, Gribben JG, Adler DA, Freedman AS, Dougery J, Nadler LM: The gene for B7, a costimulatory signal for T cell activation, maps to chromosomal region 3q13.3-3q21. Blood 1992, 79:489-494.
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58
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0029071696
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CD28/CTLA-4 ligands: The gene encoding CD86 B70.B7.2 maps to the same region as C080 (B7.B7.1) gene in human chromosome 3ql3-q23
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Fernandez-Ruiz E, Sornoza C, Sanchez-Madnd F, tarier L: CD28/CTLA-4 ligands: the gene encoding CD86 B70.B7.2) maps to the same region as C080 (B7.B7.1) gene in human chromosome 3ql3-q23. Eur J Immune! 1995, 25:1453-1456.
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Davies JL, Kawaguchi Y, Bennet ST, Copeman JB, Cordeil HJ, Pritchard LE, Reed PW, Gough SCL, Jenkins SC, Palmer SM et ai: A genome-wide search for human type 1 diabetes susceptibility genes. Nature 1994, 371:130-136.
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Aod1- The immunoregulatory locus controlling abrogation of tolerance in neonatal thymectomy-induced autoimmune ovarian dysgenesis, maps to mouse chromosome 16
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Wardell BB, Michael SD, Tung KS, Todd JA, Blankenhorn EP, McEntee K, Sudweeks JD, Hansen WK, Meeker ND, Griffith JS ef a/.: Aod1- the immunoregulatory locus controlling abrogation of tolerance in neonatal thymectomy-induced autoimmune ovarian dysgenesis, maps to mouse chromosome 16. Proc Nat/ Acad Sei USA 1995, 92:4758-4762.
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-5). The study describes a polymorphism in exon 1 of the CTLA-4 gene that results in a threonine→alanine substitution in the leader peptide and a change in length of a microsatellite (AT)n repeat in the 3′ untranslated region which might affect mRNA stability.
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