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. 2012:2012:819467.
doi: 10.1155/2012/819467. Epub 2011 Nov 15.

Th17 response and inflammatory autoimmune diseases

Affiliations

Th17 response and inflammatory autoimmune diseases

Janelle C Waite et al. Int J Inflam. 2012.

Abstract

The proinflammatory activity of T helper 17 (Th17) cells can be beneficial to the host during infection. However, uncontrolled or inappropriate Th17 activation has been linked to several autoimmune and autoinflammatory pathologies. Indeed, preclinical and clinical data show that Th17 cells are associated with several autoimmune diseases such as arthritis, multiple sclerosis, psoriasis, and lupus. Furthermore, targeting the interleukin-17 (IL-17) pathway has attenuated disease severity in preclinical models of autoimmune diseases. Interestingly, a recent report brings to light a potential role for Th17 cells in the autoinflammatory disorder adult-onset Still's disease (AOSD). Whether Th17 cells are the cause or are directly involved in AOSD remains to be shown. In this paper, we discuss the biology of Th17 cells, their role in autoimmune disease development, and in AOSD in particular, as well as the growing interest of the pharmaceutical industry in their use as therapeutic targets.

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Figures

Figure 1
Figure 1
Implications of Th17 differentiation in the development of the immune response.
Figure 2
Figure 2
Linking Th17 cells and IL-17 to infection and autoimmunity.

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References

    1. Harrington LE, Hatton RD, Mangan PR, et al. Interleukin 17-producing CD4+ effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages. Nature Immunology. 2005;6(11):1123–1132. - PubMed
    1. Langrish CL, Chen Y, Blumenschein WM, et al. IL-23 drives a pathogenic T cell population that induces autoimmune inflammation. Journal of Experimental Medicine. 2005;201(2):233–240. - PMC - PubMed
    1. Park H, Li Z, Yang XO, et al. A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17. Nature Immunology. 2005;6(11):1133–1141. - PMC - PubMed
    1. Chung Y, Chang SH, Martinez GJ, et al. Critical regulation of early Th17 cell differentiation by interleukin-1 signaling. Immunity. 2009;30(4):576–587. - PMC - PubMed
    1. Hirahara K, Ghoreschi K, Laurence A, Yang XP, Kanno Y, O’Shea JJ. Signal transduction pathways and transcriptional regulation in Th17 cell differentiation. Cytokine and Growth Factor Reviews. 2010;21(6):425–434. - PMC - PubMed

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