Multiple paths to loss of anergy and gain of autoimmunity

References

• Nemazee D. Can receptor editing play an important role in normal B-cell development?. J Autoimmun 1996; 9(2)259–261
   PubMedGoogle Scholar
• Wardemann H, et al. Predominant autoantibody production by early human B cell precursors. Science 2003; 301(5638)1374–1377
   PubMed Web of Science ®Google Scholar
• Casellas R, et al. Contribution of receptor editing to the antibody repertoire. Science 2001; 291(5508)1541–1544
   PubMedGoogle Scholar
• Benschop RJ, et al. Unique signaling properties of B cell antigen receptor in mature and immature B cells: Implications for tolerance and activation. J Immunol 2001; 167(8)4172–4179
   PubMedGoogle Scholar
• Goodnow CC, et al. Self-tolerance checkpoints in B lymphocyte development. Adv Immunol 1995; 59: 279–368
   PubMed Web of Science ®Google Scholar
• Lang J, et al. Enforced Bcl-2 expression inhibits antigen-mediated clonal elimination of peripheral B cells in an antigen dose-dependent manner and promotes receptor editing in autoreactive, immature B cells. J Exp Med 1997; 186(9)1513–1522
   PubMed Web of Science ®Google Scholar
• Benschop RJ, et al. Activation and anergy in bone marrow B cells of a novel immunoglobulin transgenic mouse that is both hapten specific and autoreactive. Immunity 2001; 14(1)33–43
   PubMedGoogle Scholar
• Allman D, et al. Resolution of three nonproliferative immature splenic B cell subsets reveals multiple selection points during peripheral B cell maturation. J Immunol 2001; 167(12)6834–6840
   PubMedGoogle Scholar
• Gauld SB, et al. Maintenance of B cell anergy requires constant antigen receptor occupancy and signaling. Nat Immunol 2005; 6(11)1160–1167
   PubMed Web of Science ®Google Scholar
• Gauld SB, KT Merrell, JC Cambier. Silencing of autoreactive B cells by anergy: A fresh perspective. Curr Opin Immunol 2006; 18(3)292–297
   PubMedGoogle Scholar
• Tedder TF, Inaoki M, Sato S. The CD19-CD21 complex regulates signal transduction thresholds governing humoral immunity and autoimmunity. Immunity 1997; 6(2)107–118
   PubMed Web of Science ®Google Scholar
• Taylor DK, et al. Loss of tolerance of anti-dsDNA B cells in mice overexpressing CD19. Mol Immunol 2006; 43(11)1776–1790
   PubMedGoogle Scholar
• Tsuchiya N, et al. Association of a functional CD19 polymorphism with susceptibility to systemic sclerosis. Arthritis Rheum 2004; 50(12)4002–4007
   PubMed Web of Science ®Google Scholar
• Saito E, et al. CD19-dependent B lymphocyte signaling thresholds influence skin fibrosis and autoimmunity in the tight-skin mouse. J Clin Invest 2002; 109(11)1453–1462
   PubMed Web of Science ®Google Scholar
• Viglianti GA, et al. Activation of autoreactive B cells by CpG dsDNA. Immunity 2003; 19(6)837–847
   PubMed Web of Science ®Google Scholar
• Christensen SR, et al. Toll-like receptor 9 controls anti-DNA autoantibody production in murine lupus. J Exp Med 2005; 202(2)321–331
   PubMedGoogle Scholar
• Ehlers M, et al. TLR9/MyD88 signaling is required for class switching to pathogenic IgG2a and 2b autoantibodies in SLE. J Exp Med 2006; 203(3)553–561
   PubMed Web of Science ®Google Scholar
• Cornall RJ, et al. Polygenic autoimmune traits: Lyn, CD22, and SHP-1 are limiting elements of a biochemical pathway regulating BCR signaling and selection. Immunity 1998; 8(4)497–508
   PubMed Web of Science ®Google Scholar
• Cyster JG, Goodnow CC. Tuning antigen receptor signaling by CD22: Integrating cues from antigens and the microenvironment. Immunity 1997; 6(5)509–517
   PubMedGoogle Scholar
• Nitschke L. The role of CD22 and other inhibitory co-receptors in B-cell activation. Curr Opin Immunol 2005; 17(3)290–297
   PubMed Web of Science ®Google Scholar
• O'Keefe TL, et al. Hyperresponsive B cells in CD22-deficient mice. Science 1996; 274(5288)798–801
   PubMed Web of Science ®Google Scholar
• Nitschke L, Tsubata T. Molecular interactions regulate BCR signal inhibition by CD22 and CD72. Trends Immunol 2004; 25(10)543–550
   PubMedGoogle Scholar
• Shultz LD, et al. “Viable motheaten”, a new allele at the motheaten locus. I. Pathology. Am J Pathol 1984; 116(2)179–192
   PubMedGoogle Scholar
• Shultz LD, Green MC. Motheaten, an immunodeficient mutant of the mouse. II. Depressed immune competence and elevated serum immunoglobulins. J Immunol 1976; 116(4)936–943
   PubMedGoogle Scholar
• Thien M, et al. Excess BAFF rescues self-reactive B cells from peripheral deletion and allows them to enter forbidden follicular and marginal zone niches. Immunity 2004; 20(6)785–798
   PubMed Web of Science ®Google Scholar
• Patke A, et al. BAFF controls B cell metabolic fitness through a PKC beta- and Akt-dependent mechanism. J Exp Med 2006; 203(11)2551–2562
   PubMedGoogle Scholar
• Pers JO, et al. BAFF overexpression is associated with autoantibody production in autoimmune diseases. Ann N Y Acad Sci 2005; 1050: 34–39
   PubMed Web of Science ®Google Scholar
• Stohl W, et al. BAFF overexpression and accelerated glomerular disease in mice with an incomplete genetic predisposition to systemic lupus erythematosus. Arthritis Rheum 2005; 52(7)2080–2091
   PubMed Web of Science ®Google Scholar
• Gauld SB, Cambier JC. Src-family kinases in B-cell development and signaling. Oncogene 2004; 23(48)8001–8006
   PubMed Web of Science ®Google Scholar
• Cherukuri A, et al. B cell signaling is regulated by induced palmitoylation of CD81. J Biol Chem 2004; 279(30)31973–31982
   PubMedGoogle Scholar
• Cherukuri A, et al. The tetraspanin CD81 is necessary for partitioning of coligated CD19/CD21-B cell antigen receptor complexes into signaling-active lipid rafts. J Immunol 2004; 172(1)370–380
   PubMedGoogle Scholar
• Brauweiler AM, Tamir I, Cambier JC. Bilevel control of B-cell activation by the inositol 5-phosphatase SHIP. Immunol Rev 2000; 176: 69–74
   PubMedGoogle Scholar
• Dal Porto JM, et al. B cell antigen receptor signaling 101. Mol Immunol 2004; 41(6–7)599–613
   PubMed Web of Science ®Google Scholar
• Songyang Z, et al. Domain-dependent function of the rasGAP-binding protein p62Dok in cell signaling. J Biol Chem 2001; 276(4)2459–2465
   PubMedGoogle Scholar
• Yamanashi Y, et al. Role of the rasGAP-associated docking protein p62(dok) in negative regulation of B cell receptor-mediated signaling. Genes Dev 2000; 14(1)11–16
   PubMedGoogle Scholar
• Pao LI, Famiglietti SJ, Cambier JC. Asymmetrical phosphorylation and function of immunoreceptor tyrosine-based activation motif tyrosines in B cell antigen receptor signal transduction. J Immunol 1998; 160(7)3305–3314
   PubMed Web of Science ®Google Scholar
• Vilen BJ, Nakamura T, Cambier JC. Antigen-stimulated dissociation of BCR mIg from Ig-alpha/Ig-beta: Implications for receptor desensitization. Immunity 1999; 10(2)239–248
   PubMedGoogle Scholar
• Hasegawa M, et al. Pathogenesis of systemic sclerosis: Altered B cell function is the key linking systemic autoimmunity and tissue fibrosis. J Dermatol Sci 2005; 39(1)1–7
   PubMedGoogle Scholar
• Sato S, et al. Altered B lymphocyte function induces systemic autoimmunity in systemic sclerosis. Mol Immunol 2004; 41(12)1123–1133
   PubMed Web of Science ®Google Scholar
• Asano N, et al. B lymphocyte signaling established by the CD19/CD22 loop regulates autoimmunity in the tight-skin mouse. Am J Pathol 2004; 165(2)641–650
   PubMed Web of Science ®Google Scholar
• Fulcher DA, et al. The fate of self-reactive B cells depends primarily on the degree of antigen receptor engagement and availability of T cell help. J Exp Med 1996; 183(5)2313–2328
   PubMed Web of Science ®Google Scholar
• Trinchieri G, Sher A. Cooperation of Toll-like receptor signals in innate immune defence. Nat Rev Immunol 2007; 7(3)179–190
   PubMed Web of Science ®Google Scholar
• Rui L, et al. Resistance to CpG DNA-induced autoimmunity through tolerogenic B cell antigen receptor ERK signaling. Nat Immunol 2003; 4(6)594–600
   PubMed Web of Science ®Google Scholar
• Pawar RD, et al. Ligands to nucleic acid-specific Toll-like receptors and the onset of lupus nephritis. J Am Soc Nephrol 2006; 17(12)3365–3373
   PubMed Web of Science ®Google Scholar
• Merrell KT, et al. Identification of anergic B cells within a wild-type repertoire. Immunity 2006; 25(6)953–962
   PubMedGoogle Scholar
• Tiller T, et al. Autoreactivity in human IgG(+) memory B cells. Immunity 2007; 26(2)205–213
   PubMed Web of Science ®Google Scholar
• Wilber A, et al. DNAse1l3 deficiency in lupus-prone MRL and NZB/W F1 mice. Clin Exp Immunol 2003; 134(1)46–52
   PubMed Web of Science ®Google Scholar
• Mitchell DA, et al. C1q deficiency and autoimmunity: The effects of genetic background on disease expression. J Immunol 2002; 168(5)2538–2543
   PubMedGoogle Scholar
• Napirei M, et al. Features of systemic lupus erythematosus in DNAse1-deficient mice. Nat Genet 2000; 25(2)177–181
   PubMed Web of Science ®Google Scholar
• Bijl M, et al. Reduced uptake of apoptotic cells by macrophages in systemic lupus erythematosus: Correlates with decreased serum levels of complement. Ann Rheum Dis 2006; 65(1)57–63
   PubMed Web of Science ®Google Scholar
• Moosig F, et al. Reduced expression of C1q-mRNA in monocytes from patients with systemic lupus erythematosus. Clin Exp Immunol 2006; 146(3)409–416
   PubMedGoogle Scholar
• Galeazzi M, et al. Dosage and characterization of circulating DNA: Present usage and possible applications in systemic autoimmune disorders. Autoimmun Rev 2003; 2(1)50–55
   PubMedGoogle Scholar
• Shin HD, et al. DNAse II polymorphisms associated with risk of renal disorder among systemic lupus erythematosus patients. J Hum Genet 2005; 50(3)107–111
   PubMedGoogle Scholar
• Hibbs ML, et al. Sustained activation of Lyn tyrosine kinase in vivo leads to autoimmunity. J Exp Med 2002; 196(12)1593–1604
   PubMed Web of Science ®Google Scholar
• Johnson SA, et al. Phosphorylated immunoreceptor signaling motifs (ITAMs) exhibit unique abilities to bind and activate Lyn and Syk tyrosine kinases. J Immunol 1995; 155(10)4596–4603
   PubMed Web of Science ®Google Scholar
• Hibbs ML, et al. Multiple defects in the immune system of Lyn-deficient mice, culminating in autoimmune disease. Cell 1995; 83(2)301–311
   PubMed Web of Science ®Google Scholar
• Nishizumi H, et al. A double-edged kinase Lyn: A positive and negative regulator for antigen receptor-mediated signals. J Exp Med 1998; 187(8)1343–1348
   PubMed Web of Science ®Google Scholar
• Daeron M, Lesourne R. Negative signaling in Fc receptor complexes. Adv Immunol 2006; 89: 39–86
   PubMed Web of Science ®Google Scholar
• Chan VW, Lowell CA, DeFranco AL. Defective negative regulation of antigen receptor signaling in Lyn-deficient B lymphocytes. Curr Biol 1998; 8(10)545–553
   PubMedGoogle Scholar
• Huck S, et al. Expression of B cell receptor-associated signaling molecules in human lupus. Autoimmunity 2001; 33(3)213–224
   PubMed Web of Science ®Google Scholar
• Liossis SN, et al. B-cell kinase lyn deficiency in patients with systemic lupus erythematosus. J Investig Med 2001; 49(2)157–165
   PubMed Web of Science ®Google Scholar
• Flores-Borja F, et al. Decreased Lyn expression and translocation to lipid raft signaling domains in B lymphocytes from patients with systemic lupus erythematosus. Arthritis Rheum 2005; 52(12)3955–3965
   PubMed Web of Science ®Google Scholar
• Mackay F, et al. BAFF AND APRIL: A tutorial on B cell survival. Annu Rev Immunol 2003; 21: 231–264
   PubMed Web of Science ®Google Scholar
• Mecklenbrauker I, et al. Regulation of B-cell survival by BAFF-dependent PKCdelta-mediated nuclear signalling. Nature 2004; 431(7007)456–461
   PubMedGoogle Scholar
• Lesley R, et al. Reduced competitiveness of autoantigen-engaged B cells due to increased dependence on BAFF. Immunity 2004; 20(4)441–453
   PubMed Web of Science ®Google Scholar
• Mecklenbrauker I, et al. Protein kinase Cdelta controls self-antigen-induced B-cell tolerance. Nature 2002; 416(6883)860–865
   PubMedGoogle Scholar
• Tangye SG, et al. BAFF, APRIL and human B cell disorders. Semin Immunol 2006; 18(5)305–317
   PubMedGoogle Scholar
• Becker-Merok A, Nikolaisen C, Nossent HC. B-lymphocyte activating factor in systemic lupus erythematosus and rheumatoid arthritis in relation to autoantibody levels, disease measures and time. Lupus 2006; 15(9)570–576
   PubMed Web of Science ®Google Scholar