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Mechanism by which HLA-DR4 regulates sex-bias of arthritis in humanized mice.

Abstract：

:HLA class II allele DRB1*0401 is associated with predisposition to Rheumatoid Arthritis in humans as well as collagen-induced arthritis in mice. Predominantly females develop arthritis in humans and DR4 transgenic mice; however the mechanism of sex-bias is still unknown. We have investigated the molecular basis by which DR4 is associated with sex-bias of arthritis. Here we show that differential antigen-specific immune mechanisms in DR4 male and female mice lead to increased susceptibility in female mice. B cells are hyperactive and present DR-restricted peptides robustly in females compared to males. Antigen-specific response showed that females produced B cell modulating cytokines like IL-13 while males produced IFNgamma. Male transgenic mice have higher number of T and B regulatory cells. An exogenous supply of 17beta estradiol in male mice led to enhanced expression of DR4 and antigen-specific response to DR4-restricted peptides. On the other hand, castration increased the incidence of arthritis. We propose that sex-bias in arthritis involves B cells and presentation of antigen by HLA-DR4 leading to activation of autoreactive cells and autoantibodies production in females, while regulatory B cells in males protect them from pathogenesis. The transgenic mice expressing RA susceptible haplotype simulate human RA and may be valuable to study gender differences observed in patients.

journal_name

J Autoimmun

journal_title

Journal of autoimmunity

authors

Behrens M,Trejo T,Luthra H,Griffiths M,David CS,Taneja V

doi

10.1016/j.jaut.2009.12.007

subject

Has Abstract

pub_date

2010-08-01 00:00:00

pages

1-9

issue

1

eissn

0896-8411

issn

1095-9157

pii

S0896-8411(09)00166-8

journal_volume

35

pub_type

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