MS4a6D Exacerbates Immunological Pathology in Experimental Viral Fulminant Hepatitis

MS4a6D Exacerbates Immunological Pathology in Experimental Viral Fulminant Hepatitis

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Author(s)

Author(s): Jianzhao Deng, Xuan Yang, Bei Zhang

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DOI: 10.18483/ijSci.1916 36 153 98-104 Volume 8 - Feb 2019

Abstract

The MS4A (membrane-spanning 4-domain family, subfamily A) family of proteins contains some members, including MS4A1, MS4A2 and MS4A3 and so on. Many MS4A family members are expressed on the cell surface of specific leukocyte subsets. And they have key roles in regulating cell activation, growth and development. However, the biological roles of many MS4A proteins is not particularly clear, such as MS4a6D. Here, we found that MS4a6D are expressed on the cell surface of Macrophages and DCs. In MHV3-infected MS4a6D-/- mice, macrophages decreased, in which the pro-inflammatory subsets decreased than their wild-type (WT) littermates. And the deletion of MS4a6D is associated with less severe damage and less viral replication in the liver. In conclusion, our results suggest that MS4a6D signaling can aggravate the immunopathological damage induced by MHV-3 infection in a mouse FH model. Our results suggest that inhibition of MS4a6D signaling pathways by an immunotherapeutic approach might be a useful treatment for FH.

Keywords

MHV3, MS4a6D, FH

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International Journal of Sciences is Open Access Journal.
This article is licensed under a Creative Commons Attribution 4.0 International (CC BY 4.0) License.
Author(s) retain the copyrights of this article, though, publication rights are with Alkhaer Publications.

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