Interaction between adipocytes and B lymphocytes in human metabolic diseases

Abstract

Diseases associated with disorders of carbohydrate and fat metabolism are widespread in the modern world. An essential factor in the pathogenesis of such diseases is the interaction between the cells of adipose tissue, adipocytes, and immune system cells. A long-term increase in glucose and fatty acids leads to adipocyte hypertrophy and increased expression of proinflammatory cytokines and adipokines by these cells. As a result, immune cells acquire a pro-inflammatory phenotype, and new leukocytes are recruited. Inflammation of adipose tissue leads to insulin resistance and stimulates the formation of atherosclerotic plaques and the development of autoimmune processes. New studies show that different groups of B lymphocytes play an essential role in the regulation of inflammation in adipose tissue. A decrease in B2 type lymphocytes suppresses the development of a number of metabolic diseases, whereas decreased numbers of regulatory B lymphocytes and B1 lymphocytes are associated with an increased pathology. Recent studies showed that adipocytes influence B lymphocyte activity both directly and by altering the activity of other immune cells. These findings provide a better understanding of the molecular mechanisms of human pathologies associated with impaired carbohydrate and lipid metabolism, such as type 2 diabetes mellitus.