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Therapeutic application of human leukocyte antigen-G1 improves atopic dermatitis-like skin lesions in mice. | LitMetric

Therapeutic application of human leukocyte antigen-G1 improves atopic dermatitis-like skin lesions in mice.

Int Immunopharmacol

Center for Research and Education on Drug Discovery, Faculty of Pharmaceutical Sciences, Hokkaido University, Kita-12, Nishi-6, Kita-ku, Sapporo 060-0812, Japan; Laboratory of Biomolecular Science, Faculty of Pharmaceutical Sciences, Hokkaido University, Kita-12, Nishi-6, Kita-ku, Sapporo 060-0812, Japan. Electronic address:

Published: September 2017

AI Article Synopsis

  • HLA-G is an immune checkpoint molecule that dampens immune responses, targeting T cells and other immune cells, making it a potential treatment for inflammatory disorders.
  • Previous research has shown that HLA-G1 and HLA-G2 treatments reduced joint swelling in a mouse model for rheumatoid arthritis.
  • This study found that administering HLA-G1 improved skin lesions in a mouse model for atopic dermatitis and reduced markers of immune response, indicating its potential as a therapeutic option for chronic inflammatory conditions.

Article Abstract

Human leukocyte antigen (HLA)-G is an immune checkpoint molecule that plays critical roles in immune response and in triggering inhibitory signaling to immune cells such as T cells, natural killer cells, and antigen-presenting cells. Thus, the application of HLA-G can be considered for treating immune response-related inflammatory disorders. We have previously reported that treatment with HLA-G1 and HLA-G2 ameliorates the joint swelling associated with collagen-induced arthritis of DBA/1 mice, an animal model for rheumatoid arthritis. In this study, we further investigated the effects of HLA-G1 on atopic dermatitis (AD), the most common inflammatory skin disorder. AD-like lesions were induced with the extract of the house dust mite Dermatophagoides farinae in NC/Nga mice. Continuous administration of HLA-G1 ameliorated the AD-like skin lesions in the mice. Furthermore, production of immunoglobulin E, interleukin (IL)-13, and IL-17A was significantly reduced in HLA-G1-treated mice, suggesting a Th2/Th17-mediated immune-inhibitory function of HLA-G1 in vivo. Our studies shed light on novel therapeutic strategies with recombinant HLA-G proteins for immune reaction-mediated chronic inflammatory disorders.

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Source
http://dx.doi.org/10.1016/j.intimp.2017.06.026DOI Listing

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