Abstract

Chandramohan Govindasamy^*

DOI : http://dx.doi.org/10.13005/ojc/400205

This review describes the imbalance of Th1 and Th2 cytokines during the onset and late complications of diabetes. Systemic inflammation at low-grade is well-known as the basal factor for the onset of diabetes. Several studies have been reported that cytokines have tremendous role in inflammation in type 1 diabetes (T1DM ) as well as type 2 diabetes (T2DM). In general, cellular-mediated immunity is stimulated by Th1 cells whereas Th2 stimulates B cell proliferation and antibody production. It is necessary to understand the role of immune cells secreting chemokines and cytokines, their involvement during the onset and the progression of diabetes particularly diabetic retinopathy/nephropathy. There is clear evidence that type 1 diabetes/autoimmune diabetes is caused by Th1/Th2 cell attacking the beta cells of the pancreas. Numerous cytokines and chemokines contribute to the inflammatory cascade, which may lead to β-cell damage . Th1 cells are the central source of interferon-γ while Th2 cells release interleukins (IL-4, IL-5 and IL-13). Other than diabetes, chronic low-grade inflammation has now stated as a risk factor of various chronic diseases such as obesity, hypertension and dyslipidaemia. In pre-diabetic conditions, the interplay of the pro and anti-inflammatory cytokines has been well understood. However, the association of inflammatory cytokines/chemokines secreted by Th1/Th2 cells in the cause and progression of type 2 diabetes is not fully understood. So, we summarize the results of the blood levels of Th1-Th2 cytokines from the different studies, and whether these cytokine/chemokines can be reported as risk factors for diabetes and their complications such as diabetic retinopathy (DR)/diabetic nephropathy(DN).

Diabetes; Diabetic nephropathy; Diabetic retinopathy; T1DM; T2DM; Th1/Th2 cytokines

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