IFN-γ receptor and STAT1 signaling in B cells are central to spontaneous germinal center formation and autoimmunity

B cell–intrinsic IFN-γ receptor signaling through STAT1 is required for the generation of spontaneous germinal centers, which can lead to pathogenic autoantibody production.

[1]  P. Marrack,et al.  Age-Associated B Cells: A T-bet–Dependent Effector with Roles in Protective and Pathogenic Immunity , 2015, The Journal of Immunology.

[2]  M. Boedigheimer,et al.  Blockade of Interferon‐γ Normalizes Interferon‐Regulated Gene Expression and Serum CXCL10 Levels in Patients With Systemic Lupus Erythematosus , 2015, Arthritis & rheumatology.

[3]  Shwetank,et al.  B Cell–Intrinsic CD84 and Ly108 Maintain Germinal Center B Cell Tolerance , 2015, The Journal of Immunology.

[4]  P. Gaffney,et al.  Lupus Risk Variant Increases pSTAT1 Binding and Decreases ETS1 Expression. , 2015, American journal of human genetics.

[5]  D. Rawlings,et al.  B cells take the front seat: dysregulated B cell signals orchestrate loss of tolerance and autoantibody production. , 2015, Current opinion in immunology.

[6]  S. Akira,et al.  B Cell–Intrinsic TLR7 Signaling Is Essential for the Development of Spontaneous Germinal Centers , 2014, The Journal of Immunology.

[7]  C. Alpers,et al.  Opposing Impact of B Cell–Intrinsic TLR7 and TLR9 Signals on Autoantibody Repertoire and Systemic Inflammation , 2014, The Journal of Immunology.

[8]  I. Sanz.  Rationale for B cell targeting in SLE , 2014, Seminars in Immunopathology.

[9]  A. DeFranco,et al.  Requirement for MyD88 Signaling in B Cells and Dendritic Cells for Germinal Center Anti-Nuclear Antibody Production in Lyn-Deficient Mice , 2014, The Journal of Immunology.

[10]  K. Morris,et al.  Interferon-γ and systemic autoimmunity. , 2013, Discovery medicine.

[11]  P. Marrack,et al.  T-box transcription factor T-bet, a key player in a unique type of B-cell activation essential for effective viral clearance , 2013, Proceedings of the National Academy of Sciences.

[12]  S. Nutt,et al.  The unique features of follicular T cell subsets , 2013, Cellular and Molecular Life Sciences.

[13]  R. Moon,et al.  A disease-associated PTPN22 variant promotes systemic autoimmunity in murine models. , 2013, The Journal of clinical investigation.

[14]  P. Marrack,et al.  TLR7 drives accumulation of ABCs and autoantibody production in autoimmune-prone mice , 2012, Immunologic Research.

[15]  C. Mohan,et al.  The Lupus-Prone NZM2410/NZW Strain–Derived Sle1b Sublocus Alters the Germinal Center Checkpoint in Female Mice in a B Cell–Intrinsic Manner , 2012, The Journal of Immunology.

[16]  Diego G. Silva,et al.  Interferon-γ excess leads to pathogenic accumulation of follicular helper T cells and germinal centers. , 2012, Immunity.

[17]  S. Bolland,et al.  Dual signaling by innate and adaptive immune receptors is required for TLR7-induced B-cell–mediated autoimmunity , 2012, Proceedings of the National Academy of Sciences.

[18]  Yijun Carrier,et al.  IL-21 Receptor Is Required for the Systemic Accumulation of Activated B and T Lymphocytes in MRL/MpJ-Faslpr/lpr/J Mice , 2012, The Journal of Immunology.

[19]  B. Diamond,et al.  Tolerogenic function of Blimp-1 in dendritic cells , 2012, The Journal of experimental medicine.

[20]  Z. Rahman.  Impaired clearance of apoptotic cells in germinal centers: implications for loss of B cell tolerance and induction of autoimmunity , 2011, Immunologic research.

[21]  B. Diamond,et al.  Tolerogenic function of Blimp-1 in dendritic cells , 2011, The Journal of Experimental Medicine.

[22]  D. Kitamura,et al.  In-vitro derived germinal centre B cells differentially generate memory B or plasma cells in vivo. , 2011, Nature communications.

[23]  S. Nutt,et al.  Germinal center B and follicular helper T cells: siblings, cousins or just good friends? , 2011, Nature Immunology.

[24]  T. Tiller,et al.  Development of self-reactive germinal center B cells and plasma cells in autoimmune FcγRIIB-deficient mice , 2010, The Journal of experimental medicine.

[25]  M. Bachmann,et al.  Cutting Edge: IL-21 and TLR Signaling Regulate Germinal Center Responses in a B Cell-Intrinsic Manner , 2010, The Journal of Immunology.

[26]  K. Toellner,et al.  IL-21 regulates germinal center B cell differentiation and proliferation through a B cell–intrinsic mechanism , 2010, The Journal of experimental medicine.

[27]  M. Linterman,et al.  IL-21 acts directly on B cells to regulate Bcl-6 expression and germinal center responses , 2010, The Journal of experimental medicine.

[28]  Sami Al-Hajjar,et al.  B cell–intrinsic signaling through IL-21 receptor and STAT3 is required for establishing long-lived antibody responses in humans , 2010, The Journal of experimental medicine.

[29]  M. Cook,et al.  Dysregulation of germinal centres in autoimmune disease , 2009, Nature Reviews Immunology.

[30]  S. Bae,et al.  Interferon-gamma gene polymorphisms associated with susceptibility to systemic lupus erythematosus , 2009, Annals of the rheumatic diseases.

[31]  T. Manser,et al.  The Lupus Susceptibility Locus Sle1 Breaches Peripheral B Cell Tolerance at the Antibody-Forming Cell and Germinal Center Checkpoints1 , 2009, The Journal of Immunology.

[32]  N. Kamatani,et al.  Excessive Production of IFN-γ in Patients with Systemic Lupus Erythematosus and Its Contribution to Induction of B Lymphocyte Stimulator/B Cell-Activating Factor/TNF Ligand Superfamily-13B1 , 2008, The Journal of Immunology.

[33]  R. Tibshirani,et al.  IRF9 and STAT1 are required for IgG autoantibody production and B cell expression of TLR7 in mice. , 2008, The Journal of clinical investigation.

[34]  P. Scott,et al.  STAT1 Expression in Dendritic Cells, but Not T Cells, Is Required for Immunity to Leishmania major1 , 2007, The Journal of Immunology.

[35]  Y. Zhang,et al.  Activation of the STAT1 signalling pathway in lupus nephritis in MRL/lpr mice , 2007, Lupus.

[36]  T. Manser,et al.  FcγRIIB Regulates Autoreactive Primary Antibody-Forming Cell, but Not Germinal Center B Cell, Activity1 , 2007, The Journal of Immunology.

[37]  S. Akira,et al.  Toll-like receptor 7-dependent loss of B cell tolerance in pathogenic autoantibody knockin mice. , 2006, Immunity.

[38]  V. Poli,et al.  Critical role for Stat3 in T-dependent terminal differentiation of IgG B cells. , 2006, Blood.

[39]  J. J. Zhang,et al.  Stat1-Dependent Synergistic Activation of T-bet for IgG2a Production during Early Stage of B Cell Activation1 , 2005, The Journal of Immunology.

[40]  A. Cappione,et al.  Germinal center exclusion of autoreactive B cells is defective in human systemic lupus erythematosus. , 2005, The Journal of clinical investigation.

[41]  H. Gascan,et al.  Direct Stimulation of Human T Cells via TLR5 and TLR7/8: Flagellin and R-848 Up-Regulate Proliferation and IFN-γ Production by Memory CD4+ T Cells1 , 2005, The Journal of Immunology.

[42]  T. Winkler,et al.  The evolution of human anti-double-stranded DNA autoantibodies. , 2005, Proceedings of the National Academy of Sciences of the United States of America.

[43]  S. Peng,et al.  Regulation of IFN-γ Production by B Effector 1 Cells: Essential Roles for T-bet and the IFN-γ Receptor1 , 2005, The Journal of Immunology.

[44]  A. Pertsemlidis,et al.  Association of extensive polymorphisms in the SLAM/CD2 gene cluster with murine lupus. , 2004, Immunity.

[45]  Y. Delneste,et al.  Direct bacterial protein PAMP recognition by human NK cells involves TLRs and triggers alpha-defensin production. , 2004, Blood.

[46]  M. Shlomchik,et al.  Activation of autoreactive B cells by CpG dsDNA. , 2003, Immunity.

[47]  Sambasiva P Rao,et al.  Normal Induction but Attenuated Progression of Germinal Center Responses in BAFF and BAFF-R Signaling–Deficient Mice , 2003, The Journal of experimental medicine.

[48]  S. Szabo,et al.  T-bet regulates IgG class switching and pathogenic autoantibody production , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[49]  M. Shlomchik,et al.  Chromatin–IgG complexes activate B cells by dual engagement of IgM and Toll-like receptors , 2002, Nature.

[50]  Chilakamarti V. Ramana,et al.  Stat1-dependent and -independent pathways in IFN-γ-dependent signaling , 2002 .

[51]  S. Shinton,et al.  Resolution of Three Nonproliferative Immature Splenic B Cell Subsets Reveals Multiple Selection Points During Peripheral B Cell Maturation1 , 2001, The Journal of Immunology.

[52]  G. Kelsoe,et al.  Spontaneous formation of germinal centers in autoimmune mice , 2001, Journal of leukocyte biology.

[53]  S. Swain,et al.  Reciprocal regulation of polarized cytokine production by effector B and T cells , 2000, Nature Immunology.

[54]  A. Csiszar,et al.  Increased interferon‐gamma (IFN‐γ), IL‐10 and decreased IL‐4 mRNA expression in peripheral blood mononuclear cells (PBMC) from patients with systemic lupus erythematosus (SLE) , 2000, Clinical and experimental immunology.

[55]  C. Smythe,et al.  Treatment of murine lupus with cDNA encoding IFN-?R/Fc , 2000 .

[56]  D. Kono,et al.  Treatment of murine lupus with cDNA encoding IFN-γR/Fc , 2000 .

[57]  M. David,et al.  Rapid STAT Phosphorylation via the B Cell Receptor , 1999, The Journal of Biological Chemistry.

[58]  A. Schwarting,et al.  IFN-gamma receptor signaling is essential for the initiation, acceleration, and destruction of autoimmune kidney disease in MRL-Fas(lpr) mice. , 1998, Journal of immunology.

[59]  B. Ryffel,et al.  IFN-γ Receptor Deletion Prevents Autoantibody Production and Glomerulonephritis in Lupus-Prone (NZB × NZW)F1 Mice , 1998, The Journal of Immunology.

[60]  B. Ryffel,et al.  IFN-gamma receptor deletion prevents autoantibody production and glomerulonephritis in lupus-prone (NZB x NZW)F1 mice. , 1998, Journal of immunology.

[61]  D. Balomenos,et al.  Interferon-gamma is required for lupus-like disease and lymphoaccumulation in MRL-lpr mice. , 1998, The Journal of clinical investigation.

[62]  N. Young,et al.  Inhibition of interferon regulatory factor-1 expression results in predominance of cell growth stimulatory effects of interferon-gamma due to phosphorylation of Stat1 and Stat3. , 1997, Blood.

[63]  B. Ryffel,et al.  Experimental therapy of systemic lupus erythematosus: the treatment of NZB/W mice with mouse soluble interferon‐γ receptor inhibits the onset of glomerulonephritis , 1995, European journal of immunology.

[64]  J D Kemp,et al.  Resolution and characterization of pro-B and pre-pro-B cell stages in normal mouse bone marrow , 1991, The Journal of experimental medicine.

[65]  H. Mcdevitt,et al.  In vivo treatment of (NZB X NZW)F1 lupus-like nephritis with monoclonal antibody to gamma interferon , 1987, The Journal of experimental medicine.

[66]  B. Diamond,et al.  The role of somatic mutation in the pathogenic anti-DNA response. , 1992, Annual review of immunology.