Autoantibody Production in Obesity: Is There Evidence for a Link Between Obesity and Autoimmunity?

PURPOSE OF REVIEW

During the last decades, obesity and autoimmune disorders have shown a parallel significant rise in industrialized countries. This review aims at providing a comprehensive update of the relationship between the adipose tissue in obesity and autoimmune disorders, highlighting the underlying mechanisms with a particular emphasis on adipokines and pro-inflammatory cytokines, the impaired B cell activity, and the production of natural and pathogenic autoantibody repertoire in the context of obesity.

RECENT FINDINGS

Obesity is related to a higher risk of rheumatoid arthritis, psoriasis and psoriatic arthritis, multiple sclerosis, and Hashimoto's thyroiditis, while it may promote inflammatory bowel disorders and type 1 diabetes mellitus. Interestingly, subjects with obesity present more severe forms of these autoimmune disorders as well as decreased therapeutic response. Both obesity and autoimmune disorders present elevated levels of leptin, resistin, and visfatin. Autoantibody production, a hallmark of autoimmune disorders, has been demonstrated in obese animal models and human subjects. Obesity results in deficiencies of the human self-tolerance mechanisms by promoting pro-inflammatory processes, reducing Bregs as well as Tregs, and the latter resulting in increased Th17 and Th1 cells, creating the perfect milieu for the development of autoimmune disorders. More mechanistic, animal, and clinical studies are required to delineate the exact mechanisms underlying auto-reactivity in obesity as well as the adipose-immune crosstalk for potential successful therapeutic strategies.