Autoimmunity as a sequela to obesity and systemic inflammation

Area of Science:

• Immunology
• Endocrinology
• Public Health

Background:

• Obesity is a global health challenge linked to severe comorbidities like cardiovascular disease, insulin resistance, and hypertension.
• Obesity-related illnesses cause millions of deaths annually, necessitating research into pathogenesis and therapeutic targets.
• Chronic inflammation and increased autoimmune disease incidence are emerging consequences of obesity.

Purpose of the Study:

• To review the mechanisms by which obesity instigates autoimmunity.
• To highlight the role of immune cell activation and adipokine secretion in obesity-driven autoimmunity.
• To identify potential therapeutic targets for obesity-associated autoimmune conditions.

Main Methods:

• Literature review of studies investigating the link between obesity and autoimmunity.
• Analysis of the role of leptin, a key adipokine, in immune system activation.
• Examination of other obesity-associated factors contributing to autoimmune pathogenesis, such as platelet activation, gut dysbiosis, and aging.

Main Results:

• Leptin, secreted by adipose tissue, enhances immune system activation, and its absence may protect against autoimmunity.
• Obesity is associated with chronic inflammation, sustained platelet activation, gut dysbiosis, and aging, all contributing to autoimmune development.
• Immune cell activation and adipokine secretion are central to how obesity triggers autoimmune responses.

Conclusions:

• Obesity significantly contributes to the development of autoimmune diseases through complex inflammatory and immune-mediated pathways.
• Leptin plays a critical role in linking obesity to autoimmunity by modulating immune responses.
• Further research into these mechanisms can lead to novel interventions for preventing and treating obesity-related autoimmune disorders.