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References

  • 1
    Cox, S. L. and Silveira, P. A., Emerging roles for B lymphocytes in Type 1 diabetes. Expert Rev. Clin. Immunol. 2009. 5: 311324.
  • 2
    Hulbert, C., Riseili, B., Rojas, M. and Thomas, J. W., B cell specificity contributes to the outcome of diabetes in nonobese diabetic mice. J. Immunol. 2001. 167: 55355538.
  • 3
    Silveira, P. A., Johnson, E., Chapman, H. D., Bui, T., Tisch, R. M. and Serreze, D. V., 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. 2002. 32: 36573666.
  • 4
    Pescovitz, M. D., Greenbaum, C. J., Krause-Steinrauf, H., Becker, D. J., Gitelman, S. E., Goland, R., Gottlieb, P. A. et al., Rituximab, B-lymphocyte depletion, and preservation of beta-cell function. N. Engl. J. Med. 2009. 361: 21432152.
  • 5
    Miao, D., Yu, L. and Eisenbarth, G. S., Role of autoantibodies in type 1 diabetes. Front. Biosci. 2007. 12: 18891898.
  • 6
    Shlomchik, M. J., Sites and stages of autoreactive B cell activation and regulation. Immunity 2008. 28: 1828.
  • 7
    Basten, A. and Brink, R., Tolerance and autoimmunity: B cells, in: Rose, N. R. and Mackay, I. R. (Eds.), The Autoimmune Diseases, 4th Edn, Academic Press, St. Louis 2006, pp. 167177.
  • 8
    Silveira, P. A., Dombrowsky, J., Johnson, E., Chapman, H. D., Nemazee, D. and Serreze, D. V., B cell selection defects underlie the development of diabetogenic APCs in nonobese diabetic mice. J. Immunol. 2004. 172: 50865094.
  • 9
    Silveira, P. A., Chapman, H. D., Stolp, J., Johnson, E., Cox, S. L., Hunter, K., Wicker, L. S. and Serreze, D. V., Genes within the Idd5 and Idd9/11 diabetes susceptibility loci affect the pathogenic activity of B cells in nonobese diabetic mice. J. Immunol. 2006. 177: 70337041.
  • 10
    Acevedo-Suarez, C. A., Hulbert, C., Woodward, E. J. and Thomas, J. W., Uncoupling of anergy from developmental arrest in anti-insulin B cells supports the development of autoimmune diabetes. J. Immunol. 2005. 174: 827833.
  • 11
    Koczwara, K., Schenker, M., Schmid, S., Kredel, K., Ziegler, A. G. and Bonifacio, E., Characterization of antibody responses to endogenous and exogenous antigen in the nonobese diabetic mouse. Clin. Immunol. 2003. 106: 155162.
  • 12
    Lesage, S., Hartley, S. B., Akkaraju, S., Wilson, J., Townsend, M. and Goodnow, C. C., Failure to censor forbidden clones of CD4 T cells in autoimmune diabetes. J. Exp. Med. 2002. 196: 11751188.
  • 13
    Akkaraju, S., Ho, W. Y., Leong, D., Canaan, K., Davis, M. M. and Goodnow, C. C., A range of CD4 T cell tolerance: partial inactivation to organ-specific antigen allows nondestructive thyroiditis or insulitis. Immunity 1997. 7: 255271.
  • 14
    Liston, A., Lesage, S., Gray, D. H., O'Reilly, L. A., Strasser, A., Fahrer, A. M., Boyd, R. L. et al., Generalized resistance to thymic deletion in the NOD mouse; a polygenic trait characterized by defective induction of Bim. Immunity 2004. 21: 817830.
  • 15
    Driver, J. P., Serreze, D. V. and Chen, Y. G., Mouse models for the study of autoimmune type 1 diabetes: a NOD to similarities and differences to human disease. Semin. Immunopathol. 2010. DOI: 10.1007/s00281-010-0204-1.
  • 16
    Merrell, K. T., Benschop, R. J., Gauld, S. B., Aviszus, K., Decote-Ricardo, D., Wysocki, L. J. and Cambier, J. C., Identification of anergic B cells within a WT repertoire. Immunity 2006. 25: 953962.
  • 17
    Cook, M. C., Basten, A. and Fazekas de St Groth, B., Outer periarteriolar lymphoid sheath arrest and subsequent differentiation of both naive and tolerant immunoglobulin transgenic B cells is determined by B cell receptor occupancy. J. Exp. Med. 1997. 186: 631643.
  • 18
    Benschop, R. J., Aviszus, K., Zhang, X., Manser, T., Cambier, J. C. and Wysocki, L. J., Activation and anergy in bone marrow B cells of a novel immunoglobulin transgenic mouse that is both hapten specific and autoreactive. Immunity 2001. 14: 3343.
  • 19
    Cyster, J. G., Hartley, S. B. and Goodnow, C. C., Competition for follicular niches excludes self-reactive cells from the recirculating B-cell repertoire. Nature 1994. 371: 389395.
  • 20
    Thien, M., Phan, T. G., Gardam, S., Amesbury, M., Basten, A., Mackay, F. and Brink, R., Excess BAFF rescues self-reactive B cells from peripheral deletion and allows them to enter forbidden follicular and marginal zone niches. Immunity 2004. 20: 785798.
  • 21
    Phan, T. G., Amesbury, M., Gardam, S., Crosbie, J., Hasbold, J., Hodgkin, P. D., Basten, A. and Brink, R., B cell receptor-independent stimuli trigger immunoglobulin (Ig) class switch recombination and production of IgG autoantibodies by anergic self-reactive B cells. J. Exp. Med. 2003. 197: 845860.
  • 22
    Cambier, J. C., Gauld, S. B., Merrell, K. T. and Vilen, B. J., B-cell anergy: from transgenic models to naturally occurring anergic B cells? Nat. Rev. Immunol. 2007. 7: 633643.
  • 23
    Akkaraju, S., Canaan, K. and Goodnow, C. C., Self-reactive B cells are not eliminated or inactivated by autoantigen expressed on thyroid epithelial cells. J. Exp. Med. 1997. 186: 20052012.
  • 24
    Rojas, M., Hulbert, C. and Thomas, J. W., Anergy and not clonal ignorance determines the fate of B cells that recognize a physiological autoantigen. J. Immunol. 2001. 166: 31943200.
  • 25
    Padlan, E. A., Silverton, E. W., Sheriff, S., Cohen, G. H., Smith-Gill, S. J. and Davies, D. R., Structure of an antibody-antigen complex: crystal structure of the HyHEL-10 Fab-lysozyme complex. Proc. Natl. Acad. Sci. USA 1989. 86: 59385942.
  • 26
    Hua, Q. X., Ladbury, J. E. and Weiss, M. A., Dynamics of a monomeric insulin analogue: testing the molten-globule hypothesis. Biochemistry 1993. 32: 14331442.
  • 27
    Ekland, E. H., Forster, R., Lipp, M. and Cyster, J. G., Requirements for follicular exclusion and competitive elimination of autoantigen-binding B cells. J. Immunol. 2004. 172: 47004708.
  • 28
    Santamaria, P., The long and winding road to understanding and conquering type 1 diabetes. Immunity 2010. 32: 437445.
  • 29
    Hussain, S. and Delovitch, T. L., Dysregulated B7-1 and B7-2 expression on nonobese diabetic mouse B cells is associated with increased T cell costimulation and the development of insulitis. J. Immunol. 2005. 174: 680687.
  • 30
    Wheat, W., Kupfer, R., Gutches, D. G., Rayat, G. R., Beilke, J., Scheinman, R. I. and Wegmann, D. R., Increased NF-kappa B activity in B cells and bone marrow-derived dendritic cells from NOD mice. Eur. J. Immunol. 2004. 34: 13951404.
  • 31
    Goodnow, C. C., Crosbie, J., Adelstein, S., Lavoie, T. B., Smith-Gill, S. J., Brink, R. A., Pritchard-Briscoe, H. et al., Altered immunoglobulin expression and functional silencing of self-reactive B lymphocytes in transgenic mice. Nature 1988. 334: 676682.
  • 32
    Goodnow, C. C., Crosbie, J., Adelstein, S., Lavoie, T. B., Smith-Gill, S. J., Brink, R. A., Pritchard-Briscoe, H. et al., Immunological tolerance in lysozyme/anti-lysozyme transgenic mice, in: Smith-Gill, S. J. and Sercarz, E. (Eds.), The Immune Response to Structurally Defined Proteins: The Lysozyme Model, Adenine Press, New York 1989, pp. 389401.
  • 33
    Zekavat, G., Mozaffari, R., Arias, V. J., Rostami, S. Y., Badkerhanian, A., Tenner, A. J., Nichols, K. E. et al., A novel CD93 polymorphism in non-obese diabetic (NOD) and NZB/W F1 mice is linked to a CD4+iNKT cell deficient state. Immunogenetics 2010. 62: 397407.