The Pathogenic Subpopulation of Th17 Cells in Obesity

(E-pub Ahead of Print)

Author(s): Natalia Todosenko, Maria Vulf*, Kristina Yurova, Daria Skuratovskaia, Olga Khaziakhmatova, Natalia Gazatova, Olga Melashchenko, Olga Urazova, Larisa Litvinova*

Journal Name: Current Pharmaceutical Design


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Abstract:

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+ Tlymphocytes 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 and is responsible for developing autoimmune reactions.

Keywords: Obesity, type 2 diabetes mellitus, non-pathogenic Th17 cells, pathogenic Th17 cells, plasticity, CD4+CD28null cells, inflammation, autoimmune disorder

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(E-pub Ahead of Print)
DOI: 10.2174/1381612826666210101154913

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