Hormonal Dysregulation and Unbalanced Specialized Pro‐Resolving Mediator Biosynthesis Contribute Toward Impaired B cell Outcomes in Obesity

Diet-induced obesity is associated with impaired B cell driven humoral immunity, which coincides with chronic inflammation and has consequences for responses to infections and vaccinations. Here we review key nutritional, cellular, and molecular mechanisms by which obesity may impair aspects of humoral immunity such as B cell development, class switch recombination, and formation of long-lived antibody secreting cells. A key theme to emerge is the central role of white adipose tissue on the formation and function of pro-inflammatory B cell subsets that exacerbate insulin resistance. We highlight the underlying role of select hormones such as leptin, which may be driving the formation of pro-inflammatory B cells in the absence of antigen stimulation. The review also extensively covers the regulatory role of lipid metabolites such as prostaglandins (PGs) and specialized pro-resolving mediators (SPMs) that are synthesized from polyunsaturated fatty acids. Notably, SPM biosynthesis is impaired in obesity and contributes toward impaired antibody production. We include future directions for research including avenues for therapeutic intervention. This article is protected by copyright. All rights reserved.