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Review
. 2013:2013:986789.
doi: 10.1155/2013/986789. Epub 2013 Dec 26.

Th17 cells in immunity and autoimmunity

Simone Kennedy Bedoya  1 , Brandon Lam  1 , Kenneth Lau  1 , Joseph Larkin 3rd  1
Affiliations
Review

Th17 cells in immunity and autoimmunity

Simone Kennedy Bedoya et al. Clin Dev Immunol. 2013.

Abstract

Th17 and IL-17 play important roles in the clearance of extracellular bacterial and fungal infections. However, strong evidence also implicates the Th17 lineage in several autoimmune disorders including multiple sclerosis, psoriasis, rheumatoid arthritis, inflammatory bowel disease, systemic lupus erythematosus, and asthma. The Th17 subset has also been connected with type I diabetes, although whether it plays a role in the pathogenicity of or protection from the disease remains a controversial issue. In this review we have provided a comprehensive overview of Th17 pathogenicity and function, including novel evidence for a protective role of Th17 cells in conjunction with the microbiota gut flora in T1D onset and progression.

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Figures

Figure 1
Figure 1
The world according to Th17 cells. Th17 cell induction occurs through combination of IL-6 and TGFβ, or IL-21 and TGFβ—in the absence of IL-6. The Th17 lineage produces cytokines which include IL-17A, IL-17F, IL-22, IL-21, GM-CSF, TNFα, IL-9, IL-10, and IFNγ. This population is enhanced through IL-23, IL-1β, TNFα, and high levels of sodium. Conversely, IL-25, IL-27, IL-2, SOCS3, SOCS1, Vitamin D, and retinoic acid serve to negatively regulate Th17 cells.
Figure 2
Figure 2
A Proposed model of bacterial regulation of T1D. Type 1 diabetes is due to the acquisition of diabetogenic effector functions by prediabetogenic T lymphocytes (T lymphocytes which bear TCR specific for pancreas related antigens have not yet been activated). Gut flora has been shown to play a critical role in immune homeostasis (see text). In this model we propose that specific microbial strains such as L. johnsonii and SFB, which naturally reside within the mucosa, can inhibit the onset of T1D by inhibiting the development of diabetogenic effector functions by T lymphocytes. While IFNγ has been associated with effector functions which lead to T1D, the work by us and others has implicated that IL17 production by T lymphocytes is associated with effector functions that are protective in T1D.
See this image and copyright information in PMC

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