Complement receptor 2/CD21− human naive B cells contain mostly autoreactive unresponsive clones

Blood - Tập 115 Số 24 - Trang 5026-5036 - 2010
Isabelle Isnardi1, Yen‐Shing Ng1, Laurence Ménard1, Greta Meyers1, David Saadoun1, Iva Srdanovic1, Jonathan Samuels1, Jessica Berman2, Jane H. Buckner3, Charlotte Cunningham‐Rundles4, Eric Meffre1
1Laboratory of Molecular Immunology, Hospital for Special Surgery, New York, NY;
2Division of Rheumatology, Hospital for Special Surgery, New York, NY;
3Translational Research Program, Benaroya Research Institute, Seattle, WA; and
4Department of Medicine and Pediatrics, Mount Sinai Medical Center, New York, NY

Tóm tắt

Abstract

Complement receptor 2–negative (CR2/CD21−) B cells have been found enriched in patients with autoimmune diseases and in common variable immunodeficiency (CVID) patients who are prone to autoimmunity. However, the physiology of CD21−/lo B cells remains poorly characterized. We found that some rheumatoid arthritis (RA) patients also display an increased frequency of CD21−/lo B cells in their blood. A majority of CD21−/lo B cells from RA and CVID patients expressed germline autoreactive antibodies, which recognized nuclear and cytoplasmic structures. In addition, these B cells were unable to induce calcium flux, become activated, or proliferate in response to B-cell receptor and/or CD40 triggering, suggesting that these autoreactive B cells may be anergic. Moreover, gene array analyses of CD21−/lo B cells revealed molecules specifically expressed in these B cells and that are likely to induce their unresponsive stage. Thus, CD21−/lo B cells contain mostly autoreactive unresponsive clones, which express a specific set of molecules that may represent new biomarkers to identify anergic B cells in humans.

Từ khóa


Tài liệu tham khảo

Nemazee, 1995, Does immunological tolerance explain the waste in the B-lymphocyte immune system? experiment and theory., Ann N Y Acad Sci, 764, 397, 10.1111/j.1749-6632.1995.tb55854.x

Radic, 1995, Origins of anti-DNA antibodies and their implications for B-cell tolerance., Ann N Y Acad Sci, 764, 384, 10.1111/j.1749-6632.1995.tb55853.x

Goodnow, 2005, Cellular and genetic mechanisms of self tolerance and autoimmunity., Nature, 435, 590, 10.1038/nature03724

Goodnow, 1988, Altered immunoglobulin expression and functional silencing of self-reactive B lymphocytes in transgenic mice., Nature, 334, 676, 10.1038/334676a0

Erikson, 1991, Expression of anti-DNA immunoglobulin transgenes in non-autoimmune mice., Nature, 349, 331, 10.1038/349331a0

Tsao, 1993, B cells are anergic in transgenic mice that express IgM anti-DNA antibodies., Eur J Immunol, 23, 2332, 10.1002/eji.1830230942

Cambier, 2007, B-cell anergy: from transgenic models to naturally occurring anergic B cells?, Nat Rev Immunol, 7, 633, 10.1038/nri2133

Fulcher, 1994, Reduced life span of anergic self-reactive B cells in a double-transgenic model., J Exp Med, 179, 125, 10.1084/jem.179.1.125

Cyster, 1994, Competition for follicular niches excludes self-reactive cells from the recirculating B-cell repertoire [see comments]., Nature, 371, 389, 10.1038/371389a0

Nemazee, 1989, Clonal deletion of B lymphocytes in a transgenic mouse bearing anti-MHC class I antibody genes., Nature, 337, 562, 10.1038/337562a0

Hartley, 1991, Elimination from peripheral lymphoid tissues of self-reactive B lymphocytes recognizing membrane-bound antigens., Nature, 353, 765, 10.1038/353765a0

Halverson, 2004, Receptor editing is the main mechanism of B cell tolerance toward membrane antigens., Nat Immunol, 5, 645, 10.1038/ni1076

Healy, 1997, Different nuclear signals are activated by the B cell receptor during positive versus negative signaling., Immunity, 6, 419, 10.1016/S1074-7613(00)80285-X

Gauld, 2005, Maintenance of B cell anergy requires constant antigen receptor occupancy and signaling., Nat Immunol, 6, 1160, 10.1038/ni1256

Merrell, 2006, Identification of anergic B cells within a wild-type repertoire., Immunity, 25, 953, 10.1016/j.immuni.2006.10.017

Duty, 2009, Functional anergy in a subpopulation of naive B cells from healthy humans that express autoreactive immunoglobulin receptors., J Exp Med, 206, 139, 10.1084/jem.20080611

Wehr, 2004, A new CD21low B cell population in the peripheral blood of patients with SLE., Clin Immunol, 113, 161, 10.1016/j.clim.2004.05.010

Wei, 2007, A new population of cells lacking expression of CD27 represents a notable component of the B cell memory compartment in systemic lupus erythematosus., J Immunol, 178, 6624, 10.4049/jimmunol.178.10.6624

Culton, 2007, Similar CD19 dysregulation in two autoantibody-associated autoimmune diseases suggests a shared mechanism of B-cell tolerance loss., J Clin Immunol, 27, 53, 10.1007/s10875-006-9051-1

Nicholas, 2008, A novel subset of memory B cells is enriched in autoreactivity and correlates with adverse outcomes in SLE., Clin Immunol, 126, 189, 10.1016/j.clim.2007.10.004

Warnatz, 2002, Severe deficiency of switched memory B cells (CD27(+)IgM(-)IgD(-)) in subgroups of patients with common variable immunodeficiency: a new approach to classify a heterogeneous disease., Blood, 99, 1544, 10.1182/blood.V99.5.1544

Warnatz, 2002, Expansion of CD19(hi)CD21(lo/neg) B cells in common variable immunodeficiency (CVID) patients with autoimmune cytopenia., Immunobiology, 206, 502, 10.1078/0171-2985-00198

Rakhmanov, 2009, Circulating CD21low B cells in common variable immunodeficiency resemble tissue homing, innate-like B cells., Proc Natl Acad Sci U S A, 106, 13451, 10.1073/pnas.0901984106

Wardemann, 2003, Predominant autoantibody production by early human B cell precursors., Science, 301, 1374, 10.1126/science.1086907

National Center for Biotechnology Information Gene Expression Omnibus (GEO). Accessed G5E, 13917 http://www.ncbi.nlm.nih.gov/geo

Cunningham-Rundles, 1999, Common variable immunodeficiency: clinical and immunological features of 248 patients., Clin Immunol, 92, 34, 10.1006/clim.1999.4725

Piqueras, 2003, Common variable immunodeficiency patient classification based on impaired B cell memory differentiation correlates with clinical aspects., J Clin Immunol, 23, 385, 10.1023/A:1025373601374

Wehr, 2008, The EUROclass trial: defining subgroups in common variable immunodeficiency., Blood, 111, 77, 10.1182/blood-2007-06-091744

Moir, 2008, Evidence for HIV-associated B cell exhaustion in a dysfunctional memory B cell compartment in HIV-infected viremic individuals., J Exp Med, 205, 1797, 10.1084/jem.20072683

Ehrhardt, 2005, Expression of the immunoregulatory molecule FcRH4 defines a distinctive tissue-based population of memory B cells., J Exp Med, 202, 783, 10.1084/jem.20050879

Ehrhardt, 2008, Discriminating gene expression profiles of memory B cell subpopulations., J Exp Med, 205, 1807, 10.1084/jem.20072682

Radic, 1993, Residues that mediate DNA binding of autoimmune antibodies., J Immunol, 150, 4966, 10.4049/jimmunol.150.11.4966

Isnardi, 2008, IRAK-4- and MyD88-dependent pathways are essential for the removal of developing autoreactive B cells in humans., Immunity, 29, 746, 10.1016/j.immuni.2008.09.015

Goodnow, 1991, Breakdown of self-tolerance in anergic B lymphocytes., Nature, 352, 532, 10.1038/352532a0

Hartley, 1993, Elimination of self-reactive B lymphocytes proceeds in two stages: arrested development and cell death., Cell, 72, 325, 10.1016/0092-8674(93)90111-3

Cooke, 1994, Immunoglobulin signal transduction guides the specificity of B cell-T cell interactions and is blocked in tolerant self-reactive B cells., J Exp Med, 179, 425, 10.1084/jem.179.2.425

Nguyen, 1997, Characterization of anti-single-stranded DNA B cells in a non-autoimmune background., J Immunol, 159, 2633, 10.4049/jimmunol.159.6.2633

Mandik-Nayak, 1997, Regulation of anti-double-stranded DNA B cells in nonautoimmune mice: localization to the T-B interface of the splenic follicle., J Exp Med, 186, 1257, 10.1084/jem.186.8.1257

Cappione, 2005, Germinal center exclusion of autoreactive B cells is defective in human systemic lupus erythematosus., J Clin Invest, 115, 3205, 10.1172/JCI24179

Pugh-Bernard, 2001, Regulation of inherently autoreactive VH4-34 B cells in the maintenance of human B cell tolerance., J Clin Invest, 108, 1061, 10.1172/JCI200112462

Charles, 2008, Clonal expansion of immunoglobulin M+CD27+ B cells in HCV-associated mixed cryoglobulinemia., Blood, 111, 1344, 10.1182/blood-2007-07-101717

Lyubchenko, 2007, Cutting edge: complement (C3d)-linked antigens break B cell anergy., J Immunol, 179, 2695, 10.4049/jimmunol.179.5.2695

Glynne, 2000, B-lymphocyte quiescence, tolerance and activation as viewed by global gene expression profiling on microarrays., Immunol Rev, 176, 216, 10.1034/j.1600-065X.2000.00614.x

Fujimoto, 1999, Modulation of B lymphocyte antigen receptor signal transduction by a CD19/CD22 regulatory loop., Immunity, 11, 191, 10.1016/S1074-7613(00)80094-1

Pan, 1999, CD72-deficient mice reveal nonredundant roles of CD72 in B cell development and activation., Immunity, 11, 495, 10.1016/S1074-7613(00)80124-7

Nimmerjahn, 2008, Fcgamma receptors as regulators of immune responses., Nat Rev Immunol, 8, 34, 10.1038/nri2206

Allen, 2004, Germinal center dark and light zone organization is mediated by CXCR4 and CXCR5., Nat Immunol, 5, 943, 10.1038/ni1100

Förster, 2008, CCR7 and its ligands: balancing immunity and tolerance., Nat Rev Immunol, 8, 362, 10.1038/nri2297

Cyster, 1995, Antigen-induced exclusion from follicles and anergy are separate and complementary processes that influence peripheral B cell fate., Immunity, 3, 691, 10.1016/1074-7613(95)90059-4

Lesley, 2004, Reduced competitiveness of autoantigen-engaged B cells due to increased dependence on BAFF., Immunity, 20, 441, 10.1016/S1074-7613(04)00079-2