Adipose Tissue Inflammation Induces B Cell Inflammation and Decreases B Cell Function in Aging

Area of Science:

• Immunology
• Gerontology
• Metabolic Diseases

Background:

• Aging is a primary risk factor for chronic diseases, with inflamm-aging (age-related chronic inflammation) potentially linking these conditions.
• Understanding the mechanisms of age-related inflammation is crucial for addressing decreased immune function in older populations.

Purpose of the Study:

• To review cellular and molecular mechanisms driving age-related inflammation.
• To examine how inflamm-aging impacts humoral immune responses, specifically antibody production, in mice and humans.
• To explore the contribution of obesity and adipose tissue to aging-related inflammation and immune dysfunction.

Main Methods:

• Literature review of published data on aging, inflammation, and immune responses.
• Analysis of cellular and molecular mechanisms contributing to inflamm-aging.
• Examination of immune cell infiltration in adipose tissue and their inflammatory roles.

Main Results:

• Aging leads to increased chronic inflammation (inflamm-aging), impairing antibody production and humoral immunity.
• Obesity exacerbates aging mechanisms through heightened inflammation, involving immune cell infiltration of adipose tissue.
• Adipose tissue harbors diverse immune cells (macrophages, T cells, B cells, etc.) that drive local and systemic inflammation.
• Leptin contributes to inflammation and reduced B cell function; adipose tissue generates pro-inflammatory B cell subsets.

Conclusions:

• Inflamm-aging, driven by mechanisms including adipose tissue dysfunction, significantly compromises immune responses, particularly antibody production.
• Obesity amplifies age-related inflammation and immune deficits, impacting B cell function and promoting insulin resistance.
• Adipose tissue-derived pro-inflammatory B cells can induce pro-inflammatory T cells and pathogenic autoimmune antibodies, contributing to age-related diseases.