T cell subsets: an integral component in pathogenesis of rheumatic heart disease

Acute rheumatic fever (ARF) is a consequence of pharyngeal infection of group A streptococcal (GAS) infection. Carditis is the most common manifestation of ARF which occurs in 30-45% of the susceptible individuals. Overlooked ARF cases might further progress towards rheumatic heart disease (RHD) in susceptible individuals, which ultimately leads to permanent heart valve damage. Molecular mimicry between streptococcal antigens and human proteins is the most widely accepted theory to describe the pathogenesis of RHD. In the recent past, various subsets of T cells have been reported to play an imperative role in the pathogenesis of RHD. Alterations in various T cell subsets, viz. Th1, Th2, Th17, and Treg cells, and their signature cytokines influence the immune responses and are associated with pathogenesis of RHD. Association of other T cell subsets (Th3, Th9, Th22, and T_FH) is not defined in context of RHD. Several investigations have confirmed the up-regulation of adhesion molecules and thus infiltration of T cells into the heart tissues. T cells secrete both Th type 1 and type 2 cytokines and these auto-reactive T cells play a key role in progression of heart valve damage. In this review, we are going to discuss about the role of T cell subsets and their corresponding cytokines in the pathogenesis of RHD.