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T cell homing to epithelial barriers in allergic disease

Abstract

Allergic inflammation develops in tissues that have large epithelial surface areas that are exposed to the environment, such as the lung, skin and gut. In the steady state, antigen-experienced memory T cells patrol these peripheral tissues to facilitate swift immune responses against invading pathogens. In at least two allergy-prone organs, the skin and the gut, memory T cells are programmed during the initial antigen priming to express trafficking receptors that enable them to preferentially home to these organs. In this review we propose that tissue-specific memory and inflammation-specific T cell trafficking facilitates the development of allergic disease in these organs. We thus review recent advances in our understanding of tissue-specific T cell trafficking and how regulation of T cell trafficking by the chemokine system contributes to allergic inflammation in mouse models and in human allergic diseases of the skin, lung and gut. Inflammation- and tissue-specific T lymphocyte trafficking pathways are currently being targeted as new treatments for non-allergic inflammatory diseases and may yield effective new therapeutics for allergic diseases.

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Figure 1: Generation of allergen-specific effector and memory T cells during primary immune responses at the epithelial barrier.
Figure 2: Tissue-specific imprinting and steady-state programmed memory T cell trafficking to atopy-prone organs.
Figure 3: Chemokine receptors associated with CD4+ helper T cell subsets.
Figure 4: Trafficking of TH2 cell subsets into the skin during the acute and chronic phases of atopic dermatitis.
Figure 5: Chemokine-regulated TH cell trafficking into the lung during the early and late phases of the asthmatic response.

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Acknowledgements

The authors were supported by US National Institutes of Health grants R37AI040618 and U19AI095261 to A.D.L.

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Islam, S., Luster, A. T cell homing to epithelial barriers in allergic disease. Nat Med 18, 705–715 (2012). https://doi.org/10.1038/nm.2760

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