有哪些信誉好的足球投注网站activation-induced cytidine deaminase deficiency causes organ-specific autoimmune diseaseactivation-induced胞嘧啶核苷脱氨酶缺乏引起瀑特异性自身免疫性疾病.pdfVIP
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activation-induced cytidine deaminase deficiency causes organ-specific autoimmune diseaseactivation-induced胞嘧啶核苷脱氨酶缺乏引起瀑特异性自身免疫性疾病
Activation-Induced Cytidine Deaminase Deficiency
Causes Organ-Specific Autoimmune Disease
1 1,2 1,2 1 3 1,2
Koji Hase , Daisuke Takahashi , Masashi Ebisawa , Sayaka Kawano , Kikuji Itoh , Hiroshi Ohno *
1 Research Center for Allergy and Immunology, RIKEN, Yokohama, Kanagawa, Japan, 2 Supramolecular Biology, International Graduate School of Arts and Sciences,
Yokohama City University, Yokohama, Kanagawa, Japan, 3 Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan
Abstract
Activation-induced cytidine deaminase (AID) expressed by germinal center B cells is a central regulator of somatic
hypermutation (SHM) and class switch recombination (CSR). Humans with AID mutations develop not only the autosomal
recessive form of hyper-IgM syndrome (HIGM2) associated with B cell hyperplasia, but also autoimmune disorders by
unknown mechanisms. We report here that AID2/ 2 mice spontaneously develop tertiary lymphoid organs (TLOs) in non-
lymphoid tissues including the stomach at around 6 months of age. At a later stage, AID2/ 2 mice develop a severe gastritis
characterized by loss of gastric glands and epithelial hyperplasia. The disease development was not attenuated even under
germ-free (GF) conditions. Gastric autoantigen -specific serum IgM was elevated in AID2/ 2 mice, and the serum levels
correlated with the gastritis pathological score. Adoptive transfer experiments suggest that autoimmune CD4+ T cells
mediate gastritis development as terminal effector cells. These results suggest that abnormal B-cell expansion due to AID
de
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