Abstract
Subclinical inflammation in morbid obesity is associated with immune activation and the development of concomitant diseases. Impaired immune homeostasis and immune cell dysregulation in adipose tissue are associated with phenotypic and functional changes in the pool of T lymphocytes and the development of chronic hypovitaminosis D. Low vitamin D levels in obesity lead to the activation, proliferation and production of pro-inflammatory mediators by T cells. Hypovitaminosis D is the cause of a decrease in the functional potential of regulatory and anti-inflammatory lymphocytes and the maintenance of the inflammatory response. The exact molecular genetic mechanisms of the effect of vitamin D on T lymphocytes have not been fully elucidated. Therefore, uncovering the functional role of T cells and their relationship to vitamin D homeostasis in the context of obesity development may contribute to the development of new pathogenetic methods for clinical prediction of the risk of metabolic, oncologic, autoimmune and infectious complications. The review presents the molecular genetic mechanisms of the effect of vitamin D on adipose tissue resident T lymphocytes and the characteristics of vitamin D receptor expression, and analyzes the phenotypic and functional characteristics of potentially pathogenic T lymphocytes in relation to the development of obesity and its associated complications.
Highlights
The pathogenesis of obesity is closely related to changes in the homeostasis of immune cells in the intestine, adipose tissue and liver [1]
Constant antigenic stimulation and a pro-inflammatory microenvironment against the background of chronic inflammation contribute to an accelerated formation of a memory T cell pool, which plays an important role in the pathogenesis of many serious diseases
It acts as an obligate heterodimer that interacts with the retinoid X receptor (RXR), which subsequently causes the translocation of the complex into the nucleus and binds in a ligand-dependent manner to the promoter regions of target genes that are sensitive to vitamin D [17,20]
Summary
The pathogenesis of obesity is closely related to changes in the homeostasis of immune cells in the intestine, adipose tissue and liver [1]. Increased expression of the P2X7 receptor in visceral and subcutaneous adipose tissue of individuals with metabolic syndrome confirms the role of adipose tissue in Th17 lymphocyte differentiation [12]. Vitamin D has been found to have a broad spectrum of functions One of these is to act directly on immune system cells by regulating their proliferation and metabolism [17]. Constant antigenic stimulation and a pro-inflammatory microenvironment against the background of chronic inflammation contribute to an accelerated formation of a memory T cell pool, which plays an important role in the pathogenesis of many serious diseases. The study of the functional role of memory T cells and their relationship with vitamin D in the context of obesity development has enormous potential and clinical significance for predicting the risk of metabolic, oncological and autoimmune complications
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
