Adaptive immunity has evolved as a very powerful and highly specialized tool of host defense. Its classical protagonists are lymphocytes of the T- and B-cell lineage. Cytokines and chemokines play a key role as effector mechanisms of the adaptive immunity. Some autoimmune and inflammatory diseases are caused by disturbance of the adaptive immune system. Recent advances in understanding the pathogenesis of autoimmune diseases have led to research on new molecular and therapeutic targets. PPARγ are members of the nuclear receptor superfamily and are transcription factors involved in lipid metabolism as well as innate and adaptive immunity. PPARγ is activated by synthetic and endogenous ligands. Previous studies have shown that PPAR agonists regulate T-cell survival, activation and T helper cell differentiation into effector subsets: Th1, Th2, Th17, and Tregs. PPARγ has also been associated with B cells. The present review addresses these issues by placing PPARγ agonists in the context of adaptive immune responses and the relation of the activation of these receptors with the expression of cytokines involved in adaptive immunity. 1. Introduction Adaptive immunity is a very powerful and specialized tool of host defense. The T- and B-cell lymphocytes are classically involved in the adaptive immune system. Disturbances of the adaptive immunity results in autoimmunity. Immune dysfunction associated with autoimmune diseases was known to be caused by an imbalance between Th1 and Th2 cells. Autoimmune diseases could be categorized as predominantly Th1-driven if the major events were cell mediated in nature, or predominantly Th2 driven if antibodies and/or immune complexes served as the main mediators [1]. In the last years, a third subset named Th17 cells has been identified, and the Th1/Th2 imbalance hypothesis has shifted to an involvement of the Th1/Th2/Th17/regulatory T (Treg) lymphocytes with the same Th precursor cells [2]. B-cell activation and antibody production can be either an independent T-cell help process or B cells receiving help from follicular T cells. In autoimmune diseases, the contact with self-antigen leads to B-cell activation and, therefore, these lineage of cells are of great importance in adaptive immunity. Naive B cells develop into antibody-producing plasma cells through the contact with antigen in combination with TLR-agonists and cytokines. Activation of B cells also results in differentiation into plasma blasts and increased cytokine production [3]. The nuclear receptor (NR) superfamily is composed of 48 members and includes
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