Mechanisms of peritoneal B-1a cells accumulation induced by murine lupus susceptibility locus Sle2

Journal of Immunology

Volumn 173, Issue 10, 2004, Pages 6050-6058

  Xu, Zhiwei ^a   Butfiloski, Edward J ^a   Sobel, Eric S ^a   Morel, Laurence ^a  

^a UNIVERSITY OF FLORIDA COLLEGE OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

B LYMPHOCYTE RECEPTOR; CARBOXYFLUORESCEIN DIACETATE SUCCINIMIDYL ESTER; CD5 ANTIGEN; IMMUNOGLOBULIN M;

ADOPTIVE TRANSFER; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; APOPTOSIS; ARTICLE; B 1A LYMPHOCYTE; B LYMPHOCYTE; BONE MARROW; CONGENIC STRAIN; CONTROLLED STUDY; FEMALE; FETUS LIVER; FLOW CYTOMETRY; GENE; GENE LOCUS; LYMPHOCYTE PROLIFERATION; MALE; MOUSE; MOUSE STRAIN; NEW ZEALAND BLACK MOUSE; NEW ZEALAND WHITE MOUSE; NONHUMAN; PERITONEUM; PRIORITY JOURNAL; RADIOSENSITIVITY; SLE2 GENE; SPLEEN; SYSTEMIC LUPUS ERYTHEMATOSUS;

EID: 8444240378     PISSN: 00221767     EISSN: None     Source Type: Journal    
DOI: 10.4049/jimmunol.173.10.6050     Document Type: Article

References (43)

1. Z homozygous inbred strains of mice derived from New-Zealand Black and New-Zealand White mice: origins and initial characterization. Lab Invest. 68:419.
2. Hayakawa, K., R. R. Hardy, D. R. Parks, and L. A. Herzenberg. 1983. The Ly-1-B cell subpopulation in normal, immunodefective, and autoimmune mice. J. Exp. Med. 157:202.
3. Mohan, C., L. Morel, P. Yang, and E. K. Wakeland. 1998. Accumulation of splenic B1a cells with potent antigen-presenting capability in NZM2410 lupus-prone mice. Arthritis Rheum. 41:1652.
4. Berland, R., and H. H. Wortis. 2002. Origins and functions of B-1 cells with notes on the role of CD5. Annu. Rev. Immunol. 20:253.
5. Blenman, K. R. M., F. R. Bahjat, L. L. Moldawer, and L. Morel. 2004. Aberrant signaling in the TNFα/TNF receptor 1 pathway of the NZM2410 lupus-prone mouse. Clin. Immunol. 110:124.
6. Reid, R. R., A. P. Prodeus, W. Khan, T. Hsu, F. S. Rosen, and M. C. Carroll. 1997. Endotoxin shock in antibody-deficient mice: unraveling the role of natural antibody and complement in the clearance of lipopolysaccharide. J. Immunol. 159:970.
7. Reap, E. A., E. S. Sobel, J. C. Jennette, P. L. Cohen, and R. A. Eisenberg. 1993. Conventional B cells, not B1 cells, are the source of autoantibodies in chronic graft-versus-host disease. J. Immunol. 151:7316.
8. Atencio, S., H. Amano, S. Izui, and B. L. Kotzin. 2004. Separation of the New Zealand Black genetic contribution to lupus from New Zealand Black determined expansions of marginal zone B and B1a cells. J. Immunol. 172:4159.
9. Murakami, M., H. Yoshioka, T. Shirai, T. Tsubata, and T. Honjo. 1995. Prevention of autoimmune symptoms in autoimmune-prone mice by elimination of B-1 cells. Int. Immunol. 7:877.
10. Iizuka, J., Y. Katagiri, N. Tada, M. Murakami, T. Ikeda, N. Sato, K. Hirokawa, S. Okada, M. Hatano, T. Tokuhisa, and T. Uede. 1998. Introduction of an osteopontin gene confers the increase in B1 cell population and the production of anti-DNA autoantibodies. Lab. Invest. 78:1523.
11. Hardy, R. R., and K. Hayakawa. 2001. B cell development pathways. Annu. Rev. Immunol. 19:595.
12. Hayakawa, K., R. R. Hardy, and L. A. Herzenberg. 1986. Peritoneal Ly-1 B-cells: genetic-control, autoantibody production, increased lambda light chain expression. Eur. J. Immunol. 16:450.
13. Hamano, Y., S. Hirose, A. Ida, M. Abe, D. Q. Zhang, S. Kodera, Y. Jiang, J. Shirai, Y. Miura, H. Nishimura, and T. Shirai. 1998. Susceptibility alleles for aberrant B-1 cell proliferation involved in spontaneously occurring B-cell chronic lymphocytic leukemia in a model of New Zealand white mice. Blood 92:3772.
14. Jiang, Y., S. Hirose, Y. Hamano, S. Kodera, H. Tsurui, M. Abe, K. Terashima, S. Ishikawa, and T. Shirai. 1997. Mapping of a gene for the increased susceptibility of B1 cells to Mott cell formation in murine autoimmune disease. J. Immunol. 158:992.
15. Xiao, W., J. He, L. Zhang, L. Li, Y. Chen, and Y. Jiang. 2003. A study of susceptibility genes mapping for aberrant B1 cell proliferation in New Zealand mice. Zhonghua Nei Ke Za Zhi. 42:38.
16. Mohan, C., L. Morel, P. Yang, and E. K. Wakeland. 1997. Genetic dissection of systemic lupus erythematosus pathogenesis: Sle2 on murine chromosome 4 leads to B cell hyperactivity. J. Immunol. 159:454.
17. Morel, L., U. H. Rudofsky, J. A. Longmate, J. Schiffenbauer, and E. K. Wakeland. 1994. Polygenic control of susceptibility to murine systemic lupus-erythematosus. Immunity 1:219.
18. Morel, L., B. P. Croker, K. R. Blenman, C. Mohan, G. L. Huang, G. Gilkeson, and E. K. Wakeland. 2000. Genetic reconstitution of systemic lupus erythematosus immunopathology with polycongenic murine strains. Proc. Natl. Acad. Sci. USA 97:6670.
19. Morel, L., Y. Yu, K. R. Blenman, R. A. Caldwell, and E. K. Wakeland. 1996. Production of congenic mouse strains carrying genomic intervals containing SLE-susceptibility genes derived from the SLE-prone NZM2410 strain. Mamm. Genome 7:335.
20. Casola, S., K. L. Otipoby, M. Alimzhanov, S. Humme, N. Uyttersprot, J. L. Kutok, M. C. Carroll, and K. Rajewsky. 2004. B cell receptor signal strength determines B cell fate. Nat. Immunol. 5:317.
21. Bikah, G., J. Carey, J. R. Ciallella, A. Tarakhovsky, and S. Bondada. 1996. CD5-mediated negative regulation of antigen receptor-induced growth signals in B-1 B cells. Science 274:1906.
22. Joliat, M. J., P. A. Lang, B. L. Lyons, L. Burzenski, M. A. Lynes, T. L. Yi, J. R. Sundberg, and L. D. Shultz. 2002. Absence of CD5 dramatically reduces progression of pulmonary inflammatory lesions in SHP-1 protein-tyrosine phosphatase-deficient 'viable motheaten' mice. J. Autoimmun. 18:105.
23. Hippen, K. L., L. E. Tze, and T. W. Behrens. 2000. CD5 maintains tolerance in anergic B cells. J. Exp. Med. 191:883.
24. Lyons, A. B., and C. R. Parrish. 1994. Determination of lymphocyte division by flow cytometry. J. Immunol. Methods 171:131.
25. Ernst, B., D. S. Lee, J. M. Chang, J. Sprent, and C. D. Surh. 1999. The peptide ligands mediating positive selection in the thymus control T cell survival and homeostatic proliferation in the periphery. Immunity 11:173.
26. Idziorek, T., J. Estaquier, F. De Bels, and J. C. Ameisen. 1995. YOPRO-1 permits cytofluorometric analysis of programmed cell death (apoptosis) without interfering with cell viability. J. Immunol. Methods 185:249.
27. Sobel, E. S., C. Mohan, L. Morel, J. Schiffenbauer, and E. K. Wakeland. 1999. Generic dissection of SLE pathogenesis: adoptive transfer of Sle1 mediates the loss of tolerance by bone marrow-derived B cells. J. Immunol. 162:2415.
28. Bondada, S., G. Bikah, D. A. Robertson, and G. Sen. 2000. Role of CD5 in growth regulation of B-1 cells. Curr. Top. Microbiol. Immunol. 252:141.
29. Solvason, N., A. Lehuen, and J. F. Kearney. 1991. An embryonic source of Ly1 but not conventional B-cells. Int. Immunol. 3:543.
30. Arnold, L. W., S. K. Mccray, C. Tatu, and S. H. Clarke. 2000. Identification of a precursor to phosphatidylcholine-specific B-1 cells suggesting that B-1 cells differentiate from splenic conventional B cells in vivo: cyclosporin A blocks differentiation to B-1. J. Immunol. 164:2924.
31. + B cells. Eur. J. Immunol. 26:2537.
32. Martin, F., and J. F. Kearney. 2000. B-cell subsets and the mature preimmune repertoire: marginal zone and B1 B cells as part of a "natural immune memory". Immunol. Rev. 175:70.
33. Hao, Z. Y., and K. Rajewsky. 2001. Homeostasis of peripheral B cells in the absence of B cell influx from the bone marrow. J. Exp. Med. 194:1151.
34. Arnold, L. W., C. A. Pennell, S. K. Mccray, and S. H. Clarke. 1994. Development of B-1 cells: segregation of phosphatidyl choline-specific B-cells to the B-1 population occurs after immunoglobulin gene expression. J. Exp. Med. 179:1585.
35. Hayakawa, K., M. Asano, S. A. Shinton, M. Gui, D. Allman, C. L. Stewart, J. Silver, and R. R. Hardy. 1999. Positive selection of natural autoreactive B cells. Science 285:113.
36. Ansel, K. M., R. B. S. Harris, and J. G. Cyster. 2002. CXCL13 is required for B1 cell homing, natural antibody production, and body cavity immunity. Immunity 16:67.
37. Deenen, G. J., and F. G. M. Kroese. 1993. Kinetics of peritoneal B-1A cells (CD5 B-cells) in young-adult mice. Eur. J. Immunol. 23:12.
38. Morris, D. L., and T. L. Rothstein. 1993. Abnormal transcription factor induction through the surface immunoglobulin-M receptor of lymphocytes-B-1. J. Exp. Med. 177:857.
39. Goodnow, C. C., J. Crosbie, S. Adelstein, T. B. Lavoie, S. J. Smithgill, R. A. Brink, H. Pritchardbriscoe, J. S. Wotherspoon, R. H. Loblay, K. Raphael, R. J. Trent, and A. Basten. 1988. Altered immunoglobulin expression and functional silencing of self-reactive lymphocytes-B in transgenic mice. Nature 334:676.
40. Fischer, G. M., L. A. Solt, W. D. Hastings, K. J. Yang, R. M. Gerstein, B. S. Nikolajczyk, S. H. Clarke, and T. L. Rothstein. 2001. Splenic and peritoneal B-1 cells differ in terms of transcriptional and proliferative features that separate peritoneal B-1 from splenic B-2 cells. Cell. Immunol. 213:62.
41. Mizuno, T., X. Zhong, and T. L. Rothstein. 2003. Fas-induced apoptosis in B cells. Apoptosis 8:451.
42. Morel, L., K. R. Blenman, B. P. Croker, and E. K. Wakeland. 2001. The major murine systemic lupus erythematosus susceptibility locus, Sle1, is a cluster of functionally related genes. Proc. Natl. Acad. Sci. USA 98:1787.
43. Croker, B. P., G. Gilkeson, and L. Morel. 2003. Genetic interactions between susceptibility loci reveal epistatic pathogenic networks in murine lupus. Genes Immun. 4:575.