The role of Th1 and Th2 in this type of disorders was quite well established. explained the relationship between practical properties of Th1 and Th2 cells and cytokines produced by them (Mosmann et al. 2005). However, in the nineties of the past century 6-Thioinosine a new cytokine, interleukin (IL)-17, was recognized (Rouvier et al. 1993; Yao et al. 1995). Consequently the presence of a novel Th cell subpopulation (Th17), able to produce IL-17, was exposed. You will find six known isoforms of IL-17, from A to F, but Th17 cells are able to produce only IL-17A and IL-17F (Tesmer et al. 2008). Both of them are pro-inflammatory cytokines. Some experts have recently demonstrated that IL-17A and/or IL-17F are responsible for development of inflammation in many disorders, especially in autoimmune diseases like rheumatoid arthritis (RA), psoriasis, juvenile idiopathic arthritis (JIA), Crohns disease and many others (Adami et al. 2014; Sizzling and Miossec 2011; Hu et al. 2011; 6-Thioinosine Rgs5 Piper et al. 2014; Tesmer et al. 2008). This unique population of CD4+ T cells generates also IL-21 (Pelletier and Girard 2007) and IL-22 (Pan et al. 2013b). Both of them are pro-inflammatory cytokines; IL-21 helps to restore the balance between Th17 and Treg cells and IL-22 is definitely a member of IL-10 cytokine family, which is definitely linked to chronic swelling and participates in pathogenesis of many autoimmune diseases. Th17, like additional Th cells, need specific cytokines and transcription factors for activation and proliferation. Specific molecules regulating Th17 cells functions and properties have become more interesting, after finding that Th17 cells take part in pathomechanisms of many diseases. Since then experts have tried to find source and function of Th17 cells and have been seeking to use them 6-Thioinosine in therapy. Today we know two ways of activation of Th17 cells and some factors, which promote and inhibit their differentiation. Th17 cells can be stimulated with the use of 6-Thioinosine IL-6/transforming growth element (TGF)- (Ghilardi and Ouyang 2007) or IL-23p40 pathway. Main inhibitors of Th17 cells are cytokines produced by Th1 and Th2 cells, interferon (IFN)- and IL-4, respectively (Stumhofer et al. 2007). Noack and Miossec (2014) have explained also Th17 reciprocally contacts with Treg human population. Cai et al. (2012) shown in mouse model, that in exosomes, TGF-1 delayed inflammatory bowel disease (IBD). At the same time, in lymph nodes, it improved proportion of Foxp3+ Tregs and decreased percentage of Th17. The connection between Th17 and Treg populations is probably extremely important in pathogenesis of autoimmune diseases, because deviation of essential balance in favor of Th17 cells significantly enhances the severity of disease. With this review, we describe recent progress in understanding of the involvement of Th17 cells and related cytokines in pathogenesis of some autoimmune diseases. To facilitate getting information about particular disorder each of them was explained separately. Finally, we emphasize recent results considering performance of therapies focusing on Th17 pathways. The Part of Th17 Cells and Related Cytokines in Pathogenesis of Autoimmune Diseases Systemic Autoimmune Diseases Substantial progress in understanding of Th17 development and the effects of IL-17 signaling in immune responses has exposed their potential part in human being autoimmune diseases. Systemic autoimmune diseases are in majority characterized by the loss of B cells control, production of autoantibodies, and formation of immune complexes, which contribute to tissue damage. Systemic Lupus Erythematosus Systemic lupus erythematosus (SLE) is definitely a chronic autoimmune disorder that may impact the skin, bones, kidneys, brain, heart, blood and additional organs. There is growing evidence in both mouse and human being models that IL-17 and Th17 cells play an important part in SLE progression. Increased quantity of T cells generating IL-17 was found in peripheral blood and inflamed organs of individuals with SLE (Crispn et al. 2008; Henriques et al. 2010; Shah et al. 2010). Plasma concentration of IL-17 was improved in new-onset individuals and during SLE flares rather than in individuals with inactive disease (Chen et al. 2010b; Henriques et al. 2010; Yang et al. 2009). Studies considering involvement of IL-17 in pathogenesis of SLE also proved that concentration of IL-17 correlates with severity of the disease (Chen et al. 2010b; Doreau et al. 2009; Shah et al..
