Obesity is a metabolic disease characterized by a chronic subclinical inflammatory response associated
with an imbalance/dysregulation of cellular homeostasis in response to excessive nutrient intake and accumulation.
CD4+ T-lymphocytes form different populations, Th1, Th2, Th9, Th17, Th22, and Treg cells, which
have phenotypic and functional differences. Despite the active study of Th17 cells in severe disorders, their role
in metabolic disorders, particularly in obesity, is not well understood. Th17 lymphocytes, depending on the microenvironment,
can form pathogenic and nonpathogenic subpopulations. Systemic inflammation induces the reprogramming
of the transcriptome of normal Th17 cells formed in epithelial tissues, which acquire new properties.
A zone of overlapping states exists between IL-17A-producing cells, which does not allow a clear
boundary between non-pathogenic Th17 and pathogenic Th17 lymphocytes. We assume that in obesity, the
pool of inflammatory pathogenic Th17 cells with cytotoxic potential is a fraction of terminally differentiated
memory lymphocytes which is responsible for developing autoimmune reactions.