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Review
. 2019 May:339:33-40.
doi: 10.1016/j.cellimm.2018.09.001. Epub 2018 Sep 17.

IL-17 and limits of success

Affiliations
Review

IL-17 and limits of success

Zahra Omidian et al. Cell Immunol. 2019 May.

Abstract

Interleukin-17 (IL-17) is a potent proinflammatory cytokine that protects a host against fungal and extracellular bacterial infections. On the other hand, excessive or dysregulated production of IL-17 underlines susceptibility to autoimmune disease. Consequently, blocking IL-17 has become an effective strategy for modulating several autoimmune diseases, including multiple sclerosis (MS), psoriasis, and rheumatoid arthritis (RA). Notably, however, IL-17 blockade remains ineffective or even pathogenic against important autoimmune diseases such as inflammatory bowel disease (IBD). Furthermore, the efficacy of IL-17 blockade against other autoimmune diseases, including type 1 diabetes (T1D) is currently unknown and waiting results of ongoing clinical trials. Coming years will determine whether the efficacy of IL-17 blockade is limited to certain autoimmune diseases or can be expanded to other autoimmune diseases. These efforts include new clinical trials aimed at testing second-generation agents with the goal of increasing the efficiency, spectrum, and ameliorating side effects of IL-17 blockade. Here we briefly review the roles of IL-17 in the pathogenesis of selected autoimmune diseases and provide updates on ongoing and recently completed trials of IL-17 based immunotherapies.

Keywords: Autoimmune diseases; Clinical trials; IL-17; Immunotherapy; Interleukin-17.

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References

    1. Fujino S, Andoh A, Bamba S, Ogawa A, Hata K, Araki Y, Bamba T, Fujiyama Y, Increased expression of interleukin 17 in inflammatory bowel disease, Gut, 52 (2003) 65–70. - PMC - PubMed
    1. Shin HC, Benbernou N, Esnault S, Guenounou M, Expression of IL-17 in human memory CD45RO+ T lymphocytes and its regulation by protein kinase A pathway, Cytokine, 11 (1999) 257–266. - PubMed
    1. Kennedy J, Rossi DL, Zurawski SM, Vega F Jr., Kastelein RA, Wagner JL, Hannum CH, Zlotnik A, Mouse IL-17: a cytokine preferentially expressed by alpha beta TCR + CD4-CD8-T cells, J Interferon Cytokine Res, 16 (1996) 611–617. - PubMed
    1. Kim JS, Jordan MS, Diversity of IL-17-producing T lymphocytes, Cell Mol Life Sci, 70 (2013) 2271–2290. - PMC - PubMed
    1. Korn T, Oukka M, Kuchroo V, Bettelli E, Th17 cells: effector T cells with inflammatory properties, Semin Immunol, 19 (2007) 362–371. - PMC - PubMed

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