核酸传感器与CD72在系统性红斑狼疮中的作用
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摘要
系统性红斑狼疮(SLE)是一种多发于青年女性的累及多个脏器的自身免疫性炎症性结缔组织疾病,其特征为机体产生针对各种细胞核抗原的自身抗体。核酸(NA)传感器在这一过程中起关键作用,一方面NA传感器可以识别微生物NA,并诱导抗微生物的免疫反应;另一方面也可以识别自身NA使B细胞产生自身抗体,同时使类浆细胞的树突状细胞产生IFN-I。CD72是一种抑制性的B细胞共受体,已有研究显示CD72可以调控SLE的发生发展。本文针对核酸传感器与CD72在系统性红斑狼疮中的作用作一简要综述,旨在为临床治疗提供参考。
Systemic lupus erythematosus(SLE) is an autoimmune inflammatory connective tissue disease that affects multiple organs in young women.It is characterized by the body's production of autoantibodies against various nuclear antigens. Nucleic acid(NA) sensors play a key role in this process. On the one hand, NA sensors can recognize microbial NA and induce anti-microbial immune responses; on the other hand, they can also recognize their own NA to make B cells produce autoantibodies while making pulp The dendritic cells of the cells produce IFN-I. CD72 is an inhibitory B cell co-receptor, and studies have shown that CD72 can regulate the development of SLE. This article provides a brief review of the role of nucleic acid sensors and CD72 in systemic lupus erythematosus, in order to provide a reference for clinical treatment.
Systemic lupus erythematosus(SLE) is an autoimmune inflammatory connective tissue disease that affects multiple organs in young women.It is characterized by the body's production of autoantibodies against various nuclear antigens. Nucleic acid(NA) sensors play a key role in this process. On the one hand, NA sensors can recognize microbial NA and induce anti-microbial immune responses; on the other hand, they can also recognize their own NA to make B cells produce autoantibodies while making pulp The dendritic cells of the cells produce IFN-I. CD72 is an inhibitory B cell co-receptor, and studies have shown that CD72 can regulate the development of SLE. This article provides a brief review of the role of nucleic acid sensors and CD72 in systemic lupus erythematosus, in order to provide a reference for clinical treatment.
引文
[1]Mohan C,Putterman C.Genetics and pathogenesis of systemic lupus erythematosus and lupus nephritis[J].Nat Rev Nephrol,2015,11(6):329-341.
[2]Christensen SR,Shupe J,Nickerson K,et al.Toll-like receptor7 and TLR9 dictate autoantibody specificity and have opposing inflammatory and regulatory roles in a murine model of lupus[J].Immunity,2006,25(3):417-428.
[3]Akatsu C,Shinagawa K,Numoto N,et al.CD72 negatively regulates B lymphocyte responses to the lupus-related endogenous toll-like receptor 7 ligand Sm/RNP[J].J Exp Med,2016,213(12):2691-2706.
[4]Funabiki M,Kato H,Miyachi Y,et al.Autoimmune disorders associated with gain of function of the intracellular sensor MDA5[J].Immunity,2014,40(2):199-212.
[5]Christensen SR,Shupe J,Nickerson K,et al.Toll-like receptor7 and TLR9 dictate autoantibody specificity and have opposing inflammatory and regulatory roles in a murine model of lupus[J].Immunity,2006,25(3):417-428.
[6]Savarese E,Steinberg C,Pawar RD,et al.Requirement of Toll-like receptor 7 for pristane-induced production of autoantibodies and development of murine lupus nephritis[J].Arthritis Rheum,2008,58(4):1107-1115.
[7]Santiago-Raber ML,Dunand-Sauthier I,Wu T,et al.Critical role of TLR7 in the acceleration of systemic lupus erythematosus in TLR9-deficient mice[J].J Autoimmun,2010,34(4):339-348.
[8]Lau CM,Broughton C,Tabor AS,et al.RNA-associated autoantigens activate B cells by combined B cell antigen receptor/Toll-like receptor 7 engagement[J].J Exp Med,2005,202(9):1171-1177.
[9]Bennett L,Palucka AK,Arce E,et al.Interferon and granulopoiesis signatures in systemic lupus erythematosus blood[J].JExp Med,2003,197(6):711-723.
[10]Baechler EC,Batliwalla FM,Karypis G,et al.Interferon-inducible gene expression signature in peripheral blood cells of patients with severe lupus[J].Proc Natl Acad Sci USA,2003,100(5):2610-2615.
[11]Kiefer K,Oropallo MA,Cancro MP,et al.Role of type I interferons in the activation of autoreactive B cells[J].Immunol Cell Biol,2012,90(5):498-504.
[12]Teichmann LL,Schenten D,Medzhitov R,et al.Signals via the adaptor MyD88 in B cells and DCs make distinct and synergistic contributions to immune activation and tissue damage in lupus[J].Immunity,2013,38(3):528-540.
[13]Hnisz D,Abraham BJ,Lee TI,et al.Super-enhancers in the control of cell identity and disease[J].Cell,2013,155(4):934-947.
[14]Hu X,Kim H,Stahl E,et al.Integrating autoimmune risk loci with gene-expression data identifies specific pathogenic immune cell subsets[J].Am J Hum Genet,2011,89(4):496-506.
[15]Namjou B,Kothari PH,Kelly JA,et al.Evaluation of the TREX1 gene in a large multi-ancestral lupus cohort[J].Genes Immun,2011,12(4):270-279.
[16]Beck-Engeser GB,Eilat D,Wabl M.An autoimmune disease prevented by anti-retroviral drugs[J].Retrovirology,2011(8):91.
[17]Gao D,Li T,Li XD,et al.Activation of cyclic GMP-AMPsynthase by self-DNA causes autoimmune diseases[J].Proc Natl Acad Sci USA,2015,112(42):E5699-E5705.
[18]Kato Y,Park J,Takamatsu H,et al.Apoptosis-derived membrane vesicles drive the cGAS-STING pathway and enhance type I IFN production in systemic lupus erythematosus[J].Ann Rheum Dis,2018,77(10):1507-1515.
[19]Adachi T,Flaswinkel H,Yakura H,et al.The B cell surface protein CD72 recruits the tyrosine phosphatase SHP-1 upon tyrosine phosphorylation[J].J Immunol,1998,160(10):4662-4665.
[20]Adachi T,Wakabayashi C,Nakayama T,et al.CD72 negatively regulates signaling through the antigen receptor of B cells[J].JImmunol,2000,164(3):1223-1229.
[21]Dustin LB,Plas DR,Wong J,et al.Expression of dominantnegative src-homology domain 2-containing protein tyrosine phosphatase-1 results in increased Syk tyrosine kinase activity and B cell activation[J].J Immunol,1999,162(5):2717-2724.
[22]Qu WM,Miyazaki T,Terada M,et al.Genetic dissection of vasculitis in MRL/lpr lupus mice:a novel susceptibility locus involving the CD72c allele[J].Eur J Immunol,2000,30(7):2027-2037.
[23]Watanabe-Fukunaga R,Brannan CI,Copeland NG,et al.Lymphoproliferation disorder in mice explained by defects in Fas antigen that mediates apoptosis[J].Nature,1992,356(6367):314-317.
[24]Li DH,Winslow MM,Cao TM,et al.Modulation of peripheral B cell tolerance by CD72 in a murine model[J].Arthritis Rheum,2008,58(10):3192-3204.
[25]Xu M,Hou R,Sato-Hayashizaki A,et al.CD72(c)is a modifier gene that regulates Fas(lpr)-induced autoimmune disease[J].JImmunol,2013,190(11):5436-5445.
[26]朱太卿.吉兰-巴雷综合征患者B淋巴细胞辅助受体CD22、CD72表达的研究[D].中南大学,2009.
[27]Tsubata T.CD22 and CD72 are inhibitory receptors dominantly expressed in B lymphocytes and regulate systemic autoimmune diseases:English version[J].Z Rheumatol,2017,76(Suppl 1):10-13.
[28]Pao LI,Lam KP,Henderson JM,et al.B cell-specific deletion of protein-tyrosine phosphatase Shp1 promotes B-1a cell development and causes systemic autoimmunity[J].Immunity,2007,27(1):35-48.
[29]Lamagna C,Hu Y,DeFranco AL,et al.B cell-specific loss of Lyn kinase leads to autoimmunity[J].J Immunol,2014,192(3):919-928.
[30]Hoffmann A,Kerr S,Jellusova J,et al.Siglec-G is a B1 cellinhibitory receptor that controls expansion and calcium signaling of the B1 cell population[J].Nat Immunol,2007,8(7):695-704.
[31]Jellusova J,Wellmann U,Amann K,et al.CD22 x Siglec-Gdouble-deficient mice have massively increased B1 cell numbers and develop systemic autoimmunity[J].J Immunol,2010,184(7):3618-3627.
[32]Takai T,Nakamura A,Endo S.Role of PIR-B in autoimmune glomerulonephritis[J].J Biomed Biotechnol,2011(2011):275302.
[33]Wilkinson R,Lyons AB,Roberts D,et al.Platelet endothelial cell adhesion molecule-1(PECAM-1/CD31)acts as a regulator of B-cell development,B-cell antigen receptor(BCR)-mediated activation,and autoimmune disease[J].Blood,2002,100(1):184-193.
[34]Brown MH,Lacey E.A ligand for CD5 is CD5[J].J Immunol,2010,185(10):6068-6074.
[35]Kumanogoh A,Watanabe C,Lee I,et al.Identification of CD72 as a lymphocyte receptor for the class IV semaphorin CD100:a novel mechanism for regulating B cell signaling[J].Immunity,2000,13(5):621-631.
[36]Macauley MS,Crocker PR,Paulson JC.Siglec-mediated regulation of immune cell function in disease[J].Nat Rev Immunol,2014,14(10):653-666.
[37]Hutzler S,Ozgor L,Naito-Matsui Y,et al.The ligand-binding domain of Siglec-G is crucial for its selective inhibitory function on B1 cells[J].J Immunol,2014,192(11):5406-5414.
[38]Vadasz Z,Goldeberg Y,Halasz K,et al.Increased soluble CD72 in systemic lupus erythematosus is in association with disease activity and lupus nephritis[J].Clin Immunol,2016(164):114-118.
[2]Christensen SR,Shupe J,Nickerson K,et al.Toll-like receptor7 and TLR9 dictate autoantibody specificity and have opposing inflammatory and regulatory roles in a murine model of lupus[J].Immunity,2006,25(3):417-428.
[3]Akatsu C,Shinagawa K,Numoto N,et al.CD72 negatively regulates B lymphocyte responses to the lupus-related endogenous toll-like receptor 7 ligand Sm/RNP[J].J Exp Med,2016,213(12):2691-2706.
[4]Funabiki M,Kato H,Miyachi Y,et al.Autoimmune disorders associated with gain of function of the intracellular sensor MDA5[J].Immunity,2014,40(2):199-212.
[5]Christensen SR,Shupe J,Nickerson K,et al.Toll-like receptor7 and TLR9 dictate autoantibody specificity and have opposing inflammatory and regulatory roles in a murine model of lupus[J].Immunity,2006,25(3):417-428.
[6]Savarese E,Steinberg C,Pawar RD,et al.Requirement of Toll-like receptor 7 for pristane-induced production of autoantibodies and development of murine lupus nephritis[J].Arthritis Rheum,2008,58(4):1107-1115.
[7]Santiago-Raber ML,Dunand-Sauthier I,Wu T,et al.Critical role of TLR7 in the acceleration of systemic lupus erythematosus in TLR9-deficient mice[J].J Autoimmun,2010,34(4):339-348.
[8]Lau CM,Broughton C,Tabor AS,et al.RNA-associated autoantigens activate B cells by combined B cell antigen receptor/Toll-like receptor 7 engagement[J].J Exp Med,2005,202(9):1171-1177.
[9]Bennett L,Palucka AK,Arce E,et al.Interferon and granulopoiesis signatures in systemic lupus erythematosus blood[J].JExp Med,2003,197(6):711-723.
[10]Baechler EC,Batliwalla FM,Karypis G,et al.Interferon-inducible gene expression signature in peripheral blood cells of patients with severe lupus[J].Proc Natl Acad Sci USA,2003,100(5):2610-2615.
[11]Kiefer K,Oropallo MA,Cancro MP,et al.Role of type I interferons in the activation of autoreactive B cells[J].Immunol Cell Biol,2012,90(5):498-504.
[12]Teichmann LL,Schenten D,Medzhitov R,et al.Signals via the adaptor MyD88 in B cells and DCs make distinct and synergistic contributions to immune activation and tissue damage in lupus[J].Immunity,2013,38(3):528-540.
[13]Hnisz D,Abraham BJ,Lee TI,et al.Super-enhancers in the control of cell identity and disease[J].Cell,2013,155(4):934-947.
[14]Hu X,Kim H,Stahl E,et al.Integrating autoimmune risk loci with gene-expression data identifies specific pathogenic immune cell subsets[J].Am J Hum Genet,2011,89(4):496-506.
[15]Namjou B,Kothari PH,Kelly JA,et al.Evaluation of the TREX1 gene in a large multi-ancestral lupus cohort[J].Genes Immun,2011,12(4):270-279.
[16]Beck-Engeser GB,Eilat D,Wabl M.An autoimmune disease prevented by anti-retroviral drugs[J].Retrovirology,2011(8):91.
[17]Gao D,Li T,Li XD,et al.Activation of cyclic GMP-AMPsynthase by self-DNA causes autoimmune diseases[J].Proc Natl Acad Sci USA,2015,112(42):E5699-E5705.
[18]Kato Y,Park J,Takamatsu H,et al.Apoptosis-derived membrane vesicles drive the cGAS-STING pathway and enhance type I IFN production in systemic lupus erythematosus[J].Ann Rheum Dis,2018,77(10):1507-1515.
[19]Adachi T,Flaswinkel H,Yakura H,et al.The B cell surface protein CD72 recruits the tyrosine phosphatase SHP-1 upon tyrosine phosphorylation[J].J Immunol,1998,160(10):4662-4665.
[20]Adachi T,Wakabayashi C,Nakayama T,et al.CD72 negatively regulates signaling through the antigen receptor of B cells[J].JImmunol,2000,164(3):1223-1229.
[21]Dustin LB,Plas DR,Wong J,et al.Expression of dominantnegative src-homology domain 2-containing protein tyrosine phosphatase-1 results in increased Syk tyrosine kinase activity and B cell activation[J].J Immunol,1999,162(5):2717-2724.
[22]Qu WM,Miyazaki T,Terada M,et al.Genetic dissection of vasculitis in MRL/lpr lupus mice:a novel susceptibility locus involving the CD72c allele[J].Eur J Immunol,2000,30(7):2027-2037.
[23]Watanabe-Fukunaga R,Brannan CI,Copeland NG,et al.Lymphoproliferation disorder in mice explained by defects in Fas antigen that mediates apoptosis[J].Nature,1992,356(6367):314-317.
[24]Li DH,Winslow MM,Cao TM,et al.Modulation of peripheral B cell tolerance by CD72 in a murine model[J].Arthritis Rheum,2008,58(10):3192-3204.
[25]Xu M,Hou R,Sato-Hayashizaki A,et al.CD72(c)is a modifier gene that regulates Fas(lpr)-induced autoimmune disease[J].JImmunol,2013,190(11):5436-5445.
[26]朱太卿.吉兰-巴雷综合征患者B淋巴细胞辅助受体CD22、CD72表达的研究[D].中南大学,2009.
[27]Tsubata T.CD22 and CD72 are inhibitory receptors dominantly expressed in B lymphocytes and regulate systemic autoimmune diseases:English version[J].Z Rheumatol,2017,76(Suppl 1):10-13.
[28]Pao LI,Lam KP,Henderson JM,et al.B cell-specific deletion of protein-tyrosine phosphatase Shp1 promotes B-1a cell development and causes systemic autoimmunity[J].Immunity,2007,27(1):35-48.
[29]Lamagna C,Hu Y,DeFranco AL,et al.B cell-specific loss of Lyn kinase leads to autoimmunity[J].J Immunol,2014,192(3):919-928.
[30]Hoffmann A,Kerr S,Jellusova J,et al.Siglec-G is a B1 cellinhibitory receptor that controls expansion and calcium signaling of the B1 cell population[J].Nat Immunol,2007,8(7):695-704.
[31]Jellusova J,Wellmann U,Amann K,et al.CD22 x Siglec-Gdouble-deficient mice have massively increased B1 cell numbers and develop systemic autoimmunity[J].J Immunol,2010,184(7):3618-3627.
[32]Takai T,Nakamura A,Endo S.Role of PIR-B in autoimmune glomerulonephritis[J].J Biomed Biotechnol,2011(2011):275302.
[33]Wilkinson R,Lyons AB,Roberts D,et al.Platelet endothelial cell adhesion molecule-1(PECAM-1/CD31)acts as a regulator of B-cell development,B-cell antigen receptor(BCR)-mediated activation,and autoimmune disease[J].Blood,2002,100(1):184-193.
[34]Brown MH,Lacey E.A ligand for CD5 is CD5[J].J Immunol,2010,185(10):6068-6074.
[35]Kumanogoh A,Watanabe C,Lee I,et al.Identification of CD72 as a lymphocyte receptor for the class IV semaphorin CD100:a novel mechanism for regulating B cell signaling[J].Immunity,2000,13(5):621-631.
[36]Macauley MS,Crocker PR,Paulson JC.Siglec-mediated regulation of immune cell function in disease[J].Nat Rev Immunol,2014,14(10):653-666.
[37]Hutzler S,Ozgor L,Naito-Matsui Y,et al.The ligand-binding domain of Siglec-G is crucial for its selective inhibitory function on B1 cells[J].J Immunol,2014,192(11):5406-5414.
[38]Vadasz Z,Goldeberg Y,Halasz K,et al.Increased soluble CD72 in systemic lupus erythematosus is in association with disease activity and lupus nephritis[J].Clin Immunol,2016(164):114-118.