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Review
. 2016 May 27:7:210.
doi: 10.3389/fimmu.2016.00210. eCollection 2016.

Chronic Inflammation and γδ T Cells

Nathan S Fay  1 , Emily C Larson  1 , Julie M Jameson  1
Affiliations
Review

Chronic Inflammation and γδ T Cells

Nathan S Fay et al. Front Immunol. .

Abstract

The epithelial tissues of the skin, lungs, reproductive tract, and intestines are the largest physical barriers the body has to protect against infection. Epithelial tissues are woven with a matrix of immune cells programed to mobilize the host innate and adaptive immune responses. Included among these immune cells are gamma delta T lymphocytes (γδ T cells) that are unique in their T cell receptor usage, location, and functions in the body. Stress reception by γδ T cells as a result of traumatic epithelial injury, malignancy, and/or infection induces γδ T cell activation. Once activated, γδ T cells function to repair tissue, induce inflammation, recruit leukocytes, and lyse cells. Many of these functions are mediated via the production of cytokines and growth factors upon γδ T cell activation. Pathogenesis of many chronic inflammatory diseases involves γδ T cells; some of which are exacerbated by their presence, while others are improved. γδ T cells require a delicate balance between their need for acute inflammatory mediators to function normally and the detrimental impact imparted by chronic inflammation. This review will focus on the recent progress made in understanding how epithelial γδ T cells influence the pathogenesis of chronic inflammatory diseases and how a balance between acute and chronic inflammation impacts γδ T cell function. Future studies will be important to understand how this balance is achieved.

Keywords: cytokines; diabetes; epithelia; inflammation; intestine; lungs; obesity; γδ T cells.

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Figures

Figure 1
Figure 1
Stress-related signals activate γδ T cells following trauma to epithelial tissues (A). CAR–JAML interaction between keratinocytes and γδ T cells (B) costimulates γδ T cell activation. Activated γδ T cells secrete growth factors to initiate tissue repair (C) and trigger macrophage (mφ) recruitment to assist in inflammation (D). γδ T cells proximal to the wound site have fewer dendrites and appear more rounded (E).
Figure 2
Figure 2
γδ T cells under chronic inflammatory conditions show reduced activity, contributing to multiple pathophysiological issues.
See this image and copyright information in PMC

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References

    1. Tschachler E, Steiner G, Yamada H, Elbe A, Wolff K, Stingl G. Dendritic epidermal T cells: activation requirements and phenotypic characterization of proliferating cells. J Invest Dermatol (1989) 92(5):763–8.10.1111/1523-1747.ep12722546 - DOI - PubMed
    1. Sharp LL, Jameson JM, Cauvi G, Havran WL. Dendritic epidermal T cells regulate skin homeostasis through local production of insulin-like growth factor 1. Nat Immunol (2005) 6(1):73–9.10.1038/ni1152 - DOI - PubMed
    1. Khairallah C, Netzer S, Villacreces A, Juzan M, Rousseau B, Dulanto S, et al. γδ T cells confer protection against murine cytomegalovirus (MCMV). PLoS Pathog (2015) 11:e1004702. - PMC - PubMed
    1. Jameson JM, Ugarte K, Chen N, Yachi P, Fuchs E, Boismenu R, et al. A role for skin gammadelta T cells in wound repair. Science (2002) 296(5568):747–9.10.1126/science.1069639 - DOI - PubMed
    1. Jameson JM, Cauvi G, Witherden DA, Havran WL. A keratinocyte-responsive gamma delta TCR is necessary for dendritic epidermal T cell activation by damaged keratinocytes and maintenance in the epidermis. J Immunol (2004) 172(6):3573–9.10.4049/jimmunol.172.6.3573 - DOI - PubMed

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