Type 1 diabetes is thought to involve chronic inflammation, which is manifested by the activation and expression of different inflammatory mediators. IL-12 and IL-18 are two cytokines that have been shown to exert strong proinflammatory activity and have been implicated in the pathogenesis of type 1 diabetes in mice and humans. The overproduction of proinflammatory mediators is controlled by specialized T cell subset, namely regulatory T cells that express FOXP3 transcription factor.
View Article and Find Full Text PDFPurpose: The study aimed to investigate the influence of estrogen receptor α (ER-α) genotypes on inflammatory response and development of microvascular complications in girls with type 1 diabetes.
Methods: 152 young regularly menstruating girls with diagnosed type 1 diabetes and 84 young, healthy menstruating girls were recruited. ER-α genotyping was carried out by PCR.
Type 1 diabetes is considered as pluricausal disease, whose etiology involves genetic predisposition as well as environmental factors that contribute to disease progression and pathogenesis. Women are believed to be more susceptible to develop autoimmune diseases, which may depend in part on the influence of sex hormones on the immune system. It was shown that estrogens may protect against the development of autoimmune disease by inducing the expansion of regulatory T cell pool and upregulating Foxp3 expression.
View Article and Find Full Text PDFThe presence of low-grade chronic inflammation is a known feature of long standing diabetes type 1. The association between serum level of several markers of inflammation and severity of DM1 was proven. Serum concentrations of TNF were reported to be elevated in diabetic patients, especially those who developed diabetic complications.
View Article and Find Full Text PDFDiabetes type 1 is a chronic autoimmune disease in which insulin-producing cells are gradually destroyed by autoreactive T cells. Human regulatory cells play important role in controlling autoimmunity, and their qualitative or quantitative dysfunctions may result in ineffective suppression of autoreactive T cells. CD62L is a surface molecule that plays role in homing capabilities of Tregs, and only cells with high expression of CD62L have high suppressive potential.
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