Cutting edge: Impaired transitional B cell production and selection in the nonobese diabetic mouse

Journal of Immunology

Volumn 176, Issue 12, 2006, Pages 7159-7164

  Quinn III, William J ^a   Noorchashm, Negin ^a   Crowley, Jenni E ^a   Reed, Amy J ^a   Noorchashm, Hooman ^a   Naji, Ali ^a   Cancro, Michael P ^a  

^a UNIVERSITY OF PENNSYLVANIA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; B LYMPHOCYTE; B LYMPHOCYTE DIFFERENTIATION; BONE MARROW; CELL ISOLATION; CELL MATURATION; CELL SELECTION; CONTROLLED STUDY; DIABETES MELLITUS; DISEASE MODEL; FLOW CYTOMETRY; KINETICS; LYMPHOCYTE MIGRATION; LYMPHOCYTE PROLIFERATION; MOUSE; MOUSE STRAIN; NONHUMAN; PRIORITY JOURNAL; TRANSITIONAL B LYMPHOCYTE;

EID: 33744924210     PISSN: 00221767     EISSN: None     Source Type: Journal    
DOI: 10.4049/jimmunol.176.12.7159     Document Type: Article

References (29)

1. Makino, S., K. Kunimoto, Y. Muraoka, Y. Mizushima, K. Katagiri, and Y. Tochino. 1980. Breeding of a non-obese, diabetic strain of mice. Jikken. Dobutsu. 29: 1-13.
2. Wicker, L. S., J. A. Todd, and L. B. Peterson. 1995. Genetic control of autoimmune diabetes in the NOD mouse. Annu. Rev. Immunol. 13: 179-200.
3. Noorchashm, H., Y. K. Lieu, N. Noorchashm, S. Y. Rostami, S. A. Greeley, A. Schlachterman, H. K. Song, L. E. Noto, A. M. Jevnikar, C. F. Barker, and A. Naji. 1999.I-Ag7-mediated antigen presentation by B lymphocytes is critical in overcoming a checkpoint in T cell tolerance to islet β cells of nonobese diabetic mice. J. Immunol. 163: 743-750.
4. Serreze, D. V., H. D. Chapman, D. S. Varnum, M. S. Hanson, P. C. Reifsnyder, S. D. Richard, S. A. Fleming, E. H. Leiter, and L. D. Shultz. 1996. B lymphocytes are essential for the initiation of T cell-mediated autoimmune diabetes: analysis of a new "speed congenic" stock of NOD.Ig mu null mice. J. Exp. Med. 184: 2049-2053.
5. Noorchashm, H., N. Noorchashm, J. Kern, S. Y. Rostami, C. F. Barker, and A. Naji. 1997. B-cells are required for the initiation of insulitis and sialitis in nonobese diabetic mice. Diabetes 46: 941-946.
6. Serreze, D. V., S. A. Fleming, H. D. Chapman, S. D. Richard, E. H. Leiter, and R. M. Tisch. 1998. B lymphocytes are critical antigen-presenting cells for the initiation of T cell-mediated autoimmune diabetes in nonobese diabetic mice. J. Immunol. 161: 3912-3918.
7. Noorchashm, H., D. J. Moore, L. E. Noto, N. Noorchashm, A. J. Reed, A. L. Reed, H. K. Song, R. Mozaffari, A. M. Jevnikar, C. F. Barker, and A. Naji. 2000. Impaired CD4 T cell activation due to reliance upon B cell-mediated costimulation in nonobese diabetic (NOD) mice. J. Immunol. 165: 4685-4696.
8. Silveira, P. A., E. Johnson, H. D. Chapman, T. Bui, R. M. Tisch, and D. V. Serreze. 2002. The preferential ability of B lymphocytes to act as diabetogenic APC in NOD mice depends on expression of self-antigen-specific immunoglobulin receptors. Eur. J. Immunol. 32: 3657-3666.
9. Greeley, S. A., D. J. Moore, H. Noorchashm, L. E. Noto, S. Y. Rostami, A. Schlachrerman, H. K. Song, B. Koeberlein, C. F. Barker, and A. Naji. 2001. Impaired activation of islet-reactive CD4 T cells in pancreatic lymph nodes of B cell-deficient nonobese diabetic mice. J. Immunol. 167: 4351-4357.
10. Yu, L., D. T. Robles, N. Abiru, P. Kaur, M. Rewers, K. Kelemen, and G. S. Eisenbarth. 2000. Early expression of antiinsulin autoantibodies of humans and the NOD mouse: evidence for early determination of subsequent diabetes. Proc. Natl. Acad. Sci. USA 97: 1701-1706.
11. Abiru, N., L. Yu, D. Miao, A. K. Maniatis, E. Liu, H. Moriyama, and G. S. Eisenbarth. 2001. Transient insulin autoantibody expression independent of development of diabetes: comparison of NOD and NOR strains. J. Autoimmun. 17: 1-6.
12. Robles, D. T., G. S. Eisenbarth, N. J. Dailey, L. B. Peterson, and L. S. Wicker. 2003. Insulin autoantibodies are associated with islet inflammation but not always related to diabetes progression in NOD congenic mice. Diabetes 52: 882-886.
13. Silveira, P. A., J. Dombrowsky, E. Johnson, H. D. Chapman, D. Nemazee, and D. V. Serreze. 2004. B cell selection defects underlie the development of diabetogenic APCs in nonobese diabetic mice. J. Immunol. 172: 5086-5094.
14. Nemazee, D., and M. Weigert. 2000. Revising B cell receptors. J. Exp. Med. 191: 1813-1817.
15. Goodnow, C. C., J. G. Cyster, S. B. Hartley, S. E. Bell, M. P. Cooke, J. I. Healy, S. Akkaraju, J. C. Rathmell, S. L. Pogue, and K. P. Shokat. 1995. Self-tolerance checkpoints in B lymphocyte development. Adv. Immunol. 59: 279-368.
16. Fulcher, D. A., and A. Basten. 1994. Reduced life span of anergic self-reactive B cells in a double-transgenic model. J. Exp. Med. 179: 125-134.
17. high splenic B cells are an immature developmental intermediate in the production of long-lived marrow-derived B cells. J. Immunol. 151: 4431-4444.
18. Srivastava, B., W. J. Quinn III, K. Hazard, J. Erikson, and D. Allman. 2005. Characterization of marginal zone B cell precursors. J. Exp. Med. 202: 1225-1234.
19. Posselt, A. M., C. F. Barker, A. L. Friedman, and A. Naji. 1992. Prevention of autoimmune diabetes in the BB rat by intrathymic islet transplantation at birth. Science 256: 1321-1324.
20. Noorchashm, H., D. J. Moore, Y. K. Lieu, N. Noorchashm, A. Schlachterman, H. K. Song, C. F. Barker, and A. Naji. 1999. Contribution of the innate immune system to autoimmune diabetes: a role for the CR1/CR2 complement receptors. Cell Immunol. 195:75-79.
21. high B lymphocytes in nonobese diabetic mice maps to diabetes susceptibility region Idd11. J. Immunol. 174: 4821-4827.
22. Agenes, F., and A. A. Freitas. 1999. Transfer of small resting B cells into immunodeficient hosts results in the selection of a self-renewing activated B cell population. J. Exp. Med. 189: 319-330.
23. Hao, Z., and K. Rajewsky. 2001. Homeostasis of peripheral B cells in the absence of B cell influx from the bone marrow. J. Exp. Med. 194: 1151-1164.
24. Thien, M., T. G. Phan, S. Gardam, M. Amesbury, A. Basten, F. Mackay, and R. Brink. 2004. Excess BAFF rescues self-reactive B cells from peripheral deletion and allows them to enter forbidden follicular and marginal zone niches. Immunity 20: 785-798.
25. Lesley, R., Y. Xu, S. L. Kalled, D. M. Hess, S. R. Schwab, H. B. Shu, and J. G. Cyster. 2004. Reduced competitiveness of autoantigen-engaged B cells due to increased dependence on BAFF. Immunity 20: 441-453.
26. Wardemann, H., S. Yurasov, A. Schaefer, J. W. Young, E. Meffre, and M. C. Nussenzweig. 2003. Predominant autoantibody production by early human B cell precursors. Science 301: 1374-1377.
27. Yurasov, S., H. Wardemann, J. Hammersen, M. Tsuiji, E. Meffre, V. Pascual, and M. C. Nussenzweig. 2005. Defective B cell tolerance checkpoints in systemic lupus erythematosus. J. Exp. Med. 201: 703-711.
28. Opstelten, D., and D. G. Osmond. 1983. Pre-B cells in mouse bone marrow: immunofluorescence stathmokinetic studies of the proliferation of cytoplasmic μ-chain-bearing cells in normal mice. J. Immunol. 131: 2635-2640.
29. Miller, J. P., J. E. Stadanlick, and M. P. Cancro. 2006. Space, selection, surveillance: setting boundaries with BLyS. J. Immunol. In press.