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Consequential differences exist between the male and female immune systems’ ability to respond to pathogens, environmental insults or self-antigens, and subsequent effects on immunoregulation.In general, females when compared with their male counterparts, respond to pathogenic stimuli and vaccines more robustly, with heightened production of antibodies, pro-inflammatory cytokines, and chemokines.The presence or absence of autoantibodies is not a reliable predictor of disease.
The high female to male incidence ratios in autoimmune diseases such as autoimmune thyroiditis, systemic lupus erythematosus (SLE), and Sjögren’s syndrome in both humans and relevant animal models have been widely reported (3–8).
Interestingly, even those diseases that did not show a strong female bias of susceptibility in the past, such as multiple sclerosis (MS), now appear to tilt toward female predisposition.
Patients diagnosed with MS were initially reported to have close to a 1:1 female:male ratio in the 1950s (9).
In this review, we describe how environmental chemicals, including EDCs, may have sex differential influence on the outcome of immune responses through alterations in epigenetic status (such as modulation of micro RNA expression, gene methylation, or histone modification status), direct and indirect activation of the estrogen receptors to drive hormonal effects, and differential modulation of microbial sensing and composition of host microbiota.
Taken together, an intriguing question develops as to how an individual’s environment directly and indirectly contributes to an altered immune response, dysregulation of autoantibody production, and influence autoimmune disease development.
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