Abstract

The end of twentieth century has introduced some changes into T helper (Th) cells division. The identification of the new subpopulation of T helper cells producing IL-17 modified model of Th1–Th2 paradigm and it was named Th17. High abilities to stimulate acute and chronic inflammation made these cells ideal candidate for crucial player in development of autoimmune disorders. Numerous publications based on animal and human models confirmed their pivotal role in pathogenesis of human systemic and organ-specific autoimmune diseases. These findings made Th17 cells and pathways regulating their development and function a good target for therapy. Therapies based on inhibition of Th17-dependent pathways are associated with clinical benefits, but on the other hand are frequently inducing adverse effects. In this review, we attempt to summarize researches focused on the importance of Th17 cells in development of human autoimmune diseases as well as effectiveness of targeting IL-17 and its pathways in pre-clinical and clinical studies.

Highlights

  • In the late twentieth century some changes in T helper cell’s classification have been introduced

  • Some researchers have recently shown that IL17A 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), Crohn’s disease and many others (Adami et al 2014; Hot and Miossec 2011; Hu et al 2011; Piper et al 2014; Tesmer et al 2008)

  • IL-17A-producing T cells are characteristically increased in peripheral blood of patients with systemic sclerosis (SSc) and they are characterized by expression of chemokine receptor CCR6 responsible for with skin- and lung-homing capabilities (Radstake et al 2009; Truchetet et al 2011)

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Summary

Introduction

In the late twentieth century some changes in T helper cell’s classification have been introduced. We attempt to summarize researches focused on the importance of Th17 cells in development of human autoimmune diseases as well as effectiveness of targeting IL-17 and its pathways in pre-clinical and clinical studies.

Results
Conclusion
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