T cells are non-conventional lymphocytes which show several properties of innate immune cells. of the epithelial barriers. T cells produce a wide range of cytokines that orchestrate the course of immune responses and also exert high cytotoxic activity against infected and transformed cells. In contrast to their beneficial role during illness, T cells will also be implicated in the development and progression of autoimmune diseases. Interestingly, several functions of T cells are susceptible to modulation by connection with additional cells. With this review, we give an overview of the T cell participation in illness and autoimmunity. We also revise the underlying mechanisms that modulate T cell function that might provide tools to control pathological immune reactions. spp., spp., spp., spp., spp., and spp.) and parasites ((Mtb), and is an extremely potent activator of V9V2 T cells (33, 34). Thanks to the presence of this metabolite, V9V2 T cells can be triggered, proliferate and create Th1-cytokines (IFN- and TNF-) (29), therefore mounting a rapid response against the microbes. Moreover, during Mtb or infections they produce IL-17 which prompts the recruitment of neutrophil and their immune response (35). In acute infections by Mtb and HMBPP-producing microbes, this cell subset expand and in re-infections they mount a secondary memory-like response (36). Furthermore, the creation of IFN- by stimulated-V9V2 T cells may donate to the immune system response against Mtb in addition to to regulate tuberculosis lesions being that they are within lung granuloma (37). V9V2 T cells also limit the introduction of intracellular Mtb with the actions of perforins, granzymes, and granulysin (20). Additionally, they are able to promote airway Compact disc8+ and Th1 Compact disc4+ replies of standard T cells specific for Mtb, through the production of IL-12 in Levomilnacipran HCl response to phosphoantigen activation (20). Inside a nonhuman primate model of Mtb illness, activation of V9V2 T cells by exogenous HMBPP up-regulates their IFN- production. This treatment promotes the inhibition of IL-22 production, which is associated with severe lesions (38). These results might be helpful to develop novel therapeutic strategies to control Mtb illness and persistence and to induce the activation of immune cells by IFN- in order to get rid of intracellular Mtb (Number ?(Figure2A2A). Open in a separate windowpane Number 2 T cells in illness and autoimmunity. (A) In response to Mtb illness, T cells produce inflammatory cytokines and exert cytotoxicity on infected cells (remaining side), related effector functions are performed in response to several viruses (ideal side). But in chronic infections T cells are less effective to control microbes. Green arrows symbolize the proposed approaches to boost the activation of T lymphocytes. (B) T cells participate in the initiation and development of autoimmune diseases. As good examples we represent pathologies in pores and skin (left side) and in CNS (right side) both having in common an axis governed by the activation of T cells and by the production of Levomilnacipran HCl IL-17 and IL-22. Figure shows different targets to block autoimmunity manifestations (red lines). RA, retinoic acid. In patients with viral infections, V3+ T cells are enriched. In hepatitis C virus (HCV) infections, it has been observed the expansion of several V3+ T cell clones in peripheral blood (39). In the liver, these cells can mount a response against virus-infected hepatocytes and non-infected host cells, suggesting that they may contribute to BP-53 the hepatic damage (40). Additionally, there is a higher frequency of IFN–producing V1+ cells, which correlates with disease evolution (41). During the immune response against viral infections, the recognition of non-classical MHC molecules by V2- T cells is determinant Levomilnacipran HCl but also participate V9V2 T cells. It has been demonstrated that activated V9V2 T cells can inhibit sub-genomic HCV replication by the production of IFN- (41, 42). In the same way, patients suffering chronic hepatitis B virus (HBV) infection, have a reduction in the circulating V2+ T cells, in the production of IFN- Levomilnacipran HCl and in the cytotoxicity mediated by T cells. These events correlate with the persistence of HBV infection (43). Noteworthy, in mouse models of infection by West Nile virus and herpes simplex virus type 2, it has been shown that T cells play a critical role in the generation of conventional CD8+ and CD4+ memory T cells, respectively (44, 45). Importantly, T cells also participate in anti-viral response early in life. It has been reported that they can mount a functional immune response to cytomegalovirus infection during development in uterus, pointing out the key role of T cells in fetal.