5B1R
Crystal structure of mouse CD72a CTLD
5B1R の概要
エントリーDOI | 10.2210/pdb5b1r/pdb |
分子名称 | B-cell differentiation antigen CD72, ACETATE ION, GLYCEROL, ... (4 entities in total) |
機能のキーワード | c-type lectin, b-cell, immune system |
由来する生物種 | Mus musculus (Mouse) |
タンパク質・核酸の鎖数 | 1 |
化学式量合計 | 15366.27 |
構造登録者 | |
主引用文献 | Akatsu, C.,Shinagawa, K.,Numoto, N.,Liu, Z.,Ucar, A.K.,Aslam, M.,Phoon, S.,Adachi, T.,Furukawa, K.,Ito, N.,Tsubata, T. CD72 negatively regulates B lymphocyte responses to the lupus-related endogenous toll-like receptor 7 ligand Sm/RNP J.Exp.Med., 213:2691-2706, 2016 Cited by PubMed Abstract: Toll-like receptor 7 (TLR7) plays an essential role in development of systemic lupus erythematosus by co-stimulating B cells reactive to the endogenous TLR7 ligand Sm/ribonucleoprotein (RNP), a crucial lupus self-antigen. However, how the TLR7-mediated autoimmune response is regulated is not yet known. In this study, we demonstrate that CD72, an inhibitory B cell co-receptor known to prevent development of lupus, recognizes Sm/RNP at the extracellular C-type lectin-like domain (CTLD) and specifically inhibits B cell response to Sm/RNP. Moreover, the CTLD of CD72, a lupus-susceptible allele, binds to Sm/RNP less strongly than that of lupus-resistant CD72 Reduced binding of CD72 is supported by x-ray crystallographic analysis that reveals a considerable alteration in charge at the putative ligand-binding site. Thus, CD72 appears to specifically inhibit B cell response to the endogenous TLR7 ligand Sm/RNP through CTLD-mediated recognition of Sm/RNP, thereby preventing production of anti-Sm/RNP antibody crucial for development of lupus. PubMed: 27810925DOI: 10.1084/jem.20160560 主引用文献が同じPDBエントリー |
実験手法 | X-RAY DIFFRACTION (1.2 Å) |
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