Obesity and susceptibility to autoimmune diseases

Abstract

For decades, obesity has been considered to be the result of the complex interaction between genes and the environment and its pathogenesis is still unresolved. The discovery of hormones and neural mediators responsible for the control of food intake and metabolism at the hypothalamic level has provided fundamental insights into the complicated pathways that control food intake. However, the molecular basis for the association between obesity and low-degree chronic inflammation is still unknown. More recently, the discovery of leptin, one of the most abundant adipocyte-derived hormones, has suggested that nutritional status, through leptin secretion, can control immune self-tolerance modulating Treg suppressive function and responsiveness. Furthermore, recent experimental evidence has shown the presence of an abundant adipose tissue-resident Treg population responsible for the control of metabolic parameters and glucose homeostasis. Better knowledge of the intricate network of interactions among leptin-related energy regulation, Treg activities and obesity could lead to valuable strategies for therapeutic intervention in obesity and obesity-associated insulin resistance.

Obesity, Type 1 Diabetes, and Psoriasis: An Autoimmune Triple Flip

“…There are strong pieces of evidence suggesting that obesity is an independent risk factor for psoriasis [113] . Furthermore, it has been indicated that obesity is more prevalent in patients with severe psoriasis than in patients with the mild form, reinforcing the link between body fat mass and psoriasis [3] . Extensive data, acquired on the proinflammatory role of adipocytes, show the pathogenic role of obesity in the incidence of psoriasis and in its severity.…”

MECHANISMS IN ENDOCRINOLOGY: The crosstalk between thyroid gland and adipose tissue: signal integration in health and disease

“…A causal link between obesity and thyroid autoimmunity has not been established so far, yet observational data from the general population suggest that obesity may increase the risk of developing allergies and several autoimmune diseases (111,112), possibly through the chronic pro-inflammatory status resulting from the accumulation of WAT in the obese patients. In obesity, the immunological tolerance can be affected both directly and indirectly, via an altered secretion of adipokines (predominantly leptin, adiponectin, and visfatin) and/or cytokines (interleukin 6 (IL6), tumor necrosis factor alpha, and interleukin 10 (IL10)).…”

“…In obesity, the immunological tolerance can be affected both directly and indirectly, via an altered secretion of adipokines (predominantly leptin, adiponectin, and visfatin) and/or cytokines (interleukin 6 (IL6), tumor necrosis factor alpha, and interleukin 10 (IL10)). The final result would be a shift from Th2 to Th1 immune response; the latter being more prone to produce autoimmune reactions (112,113,114). The visceral adipose tissue (VAT) contains resident macrophages, endothelial cells, and T cells with biased T cell receptors, which may contribute to mount an immune response by producing excessive amounts of pro-inflammatory cytokines (115).…”

Thyroid autoimmunity as a window to autoimmunity: An explanation for sex differences in the prevalence of thyroid autoimmunity

“…Also, miRNA expression has been seen to show sex differences, providing yet another potential avenue for sex differences (reviewed in Dai and Ahmed (2014)). Associations between AITDs and type 2 diabetes (Coller andHuggins, 1927 andProcaccini et al, 2011) and suggestions that inflammation may be at the core of both and responsible for the sex differences in incidence (Thorand et al, 2007).…”