5B1R

Crystal structure of mouse CD72a CTLD

Summary for 5B1R

• Entry DOI: 10.2210/pdb5b1r/pdb
• Descriptor: B-cell differentiation antigen CD72, ACETATE ION, GLYCEROL, ... (4 entities in total)
• Functional Keywords: c-type lectin, b-cell, immune system
• Biological source: Mus musculus (Mouse)
• Total number of polymer chains: 1
• Total formula weight: 15366.27

Authors

Shinagawa, K.,Numoto, N.,Tsubata, T.,Ito, N. (deposition date: 2015-12-15, release date: 2016-10-19, Last modification date: 2024-10-23)

Primary citation

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

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: 27810925
DOI: 10.1084/jem.20160560

Experimental method

X-RAY DIFFRACTION (1.2 Å)