Therapeutic effects of soluble human leukocyte antigen G2 isoform in lupus-prone MRL/lpr mice

• Watanabe, Hiroshi

• Kuroki, Kimiko

• Yamada, Chisato

• Saburi, Yukari

• Maeda, Naoyoshi

• Maenaka, Katsumi

Abstract

Human leukocyte antigen (HLA)-G, a non-classical HLA class I molecule, has one of the splicing isoforms, HLA-G2, which lacks one domain (alpha 2) and forms a non-covalent homodimer. HLA-G2 is expressed on placental cells, regulatory T cells, tumor cells, and virus-infected cells, and is involved in immunosuppression. The major isoform of HLA-G, HLA-G1, binds to leukocyte immunoglobulin (Ig)-like receptor (LILR) B1 and LILRB2, on the contrary, HLA-G2 binds to only LILRB2. We previously reported that HLA-G2 bound LILRB2 more strongly than HLA-G1 and also to paired Ig-like receptor (PIR)-B, a mouse homolog of LILRBs. Furthermore, HLA-G2 showed immunosuppressive effects in both collagen-induced arthritis (CIA) and atopic dermatitis-like model mice. In this study, we examine in vivo effects of HLA-G2 in systemic lupus erythematosus (SLE) model mice. HLA-G2 showed the suppression of the typical SLE symptoms such as serum anti-dsDNA antibody level and urinary albumin index. Furthermore, HLA-G2 tended to downregulate B-lymphocyte stimulator (BLyS) production. This is the first observation of the immunosuppressive effects of HLA-G2 isoform in SLE model mice, suggesting that HLA-G2 could be a useful therapeutic agent for SLE.

Journal

• Human immunology

  Human immunology 81 (4), 186-190, 2020-04

  Elsevier

Keywords

• HLA-G2
• LILRB2
• PIR-B
• APCs
• SLE

Details

• CRID: 1050288060491465600
• NII Article ID: 120007034052
• DOI: 10.1016/j.humimm.2019.11.002
• HANDLE: 2115/81221
• ISSN: 01988859
• Web Site: https://api.elsevier.com/content/article/PII:S0198885919311346?httpAccept=text/xml
• Web Site: https://api.elsevier.com/content/article/PII:S0198885919311346?httpAccept=text/plain
• Text Lang: en
• Article Type: journal article
• Data Source:
  • IRDB
  • Crossref
  • CiNii Articles
  • KAKEN