Literature DB >> 23518141

Human mast cells drive memory CD4+ T cells toward an inflammatory IL-22+ phenotype.

Nicolas Gaudenzio1, Camille Laurent, Salvatore Valitutti, Eric Espinosa.   

Abstract

BACKGROUND: Mast cells are key components of the skin microenvironment in psoriasis, yet their functional role in this T-cell-mediated inflammatory disorder remains to be elucidated.
OBJECTIVE: To define the impact of T-cell/mast-cell cognate interactions on the cytokines produced by TH cells.
METHODS: We used human primary mast cells and effector/memory CD4(+) T cells for in vitro coculture experiments, and we analyzed TH cells responses by using cytometry. CD4(+) T-cell/mast-cell conjugates in skin lesions from patients with psoriasis were analyzed by using 3-color immunohistochemistry and confocal microscopy.
RESULTS: We show that IFN-γ-primed human mast cells formed productive immunologic synapses with antigen-experienced CD4(+) T cells. These interactions promoted the generation of TH22 and IL-22/IFN-γ-producing TH cells from the circulating memory CD4(+) T-cell pool via a TNF-α/IL-6-dependent mechanism. An analysis of human psoriatic skin biopsies showed a rich infiltrate of IL-22(+)CD4(+) T cells frequently found in contact with mast cells. Moreover, most of these mast-cell-conjugated lymphocytes coexpressed IFN-γ, suggesting that IL-22(+)IFN-γ(+) CD4(+) T cells are generated in vivo on interaction with mast cells.
CONCLUSIONS: Our findings identify human mast cells as functional partners of TH cells, shaping their responses toward IL-22 production.
Copyright © 2013 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved.

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Year:  2013        PMID: 23518141     DOI: 10.1016/j.jaci.2013.01.029

Source DB:  PubMed          Journal:  J Allergy Clin Immunol        ISSN: 0091-6749            Impact factor:   10.793


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