Literature DB >> 22561834

T cell homing to epithelial barriers in allergic disease.

Sabina A Islam1, Andrew D Luster.   

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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Year:  2012        PMID: 22561834      PMCID: PMC3863331          DOI: 10.1038/nm.2760

Source DB:  PubMed          Journal:  Nat Med        ISSN: 1078-8956            Impact factor:   87.241


  167 in total

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Authors:  Jing-Long Huang; Pei-Song Gao; Rasika A Mathias; Tsung-Chieh Yao; Li-Chen Chen; Ming-Ling Kuo; Shih-Chang Hsu; Beverly Plunkett; Alkis Togias; Kathleen C Barnes; Cristiana Stellato; Terri H Beaty; Shau-Ku Huang
Journal:  Hum Mol Genet       Date:  2004-09-02       Impact factor: 6.150

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Review 6.  The route to pathologies in chronic inflammatory diseases characterized by T helper type 2 immune cells.

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10.  Brefeldin A reduces tumor necrosis factor-α-stimulated production of inflammatory mediators by suppressing the Akt, mTOR, and NF-κB pathways in human keratinocytes.

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