Driving IL-17+ γδ T-cell migration in allergic reactions: A new “inflammatory” role for the “homeostatic” chemokine CCL25

Authors

  • Bruno Silva-Santos

    Corresponding author
    1. Instituto de Medicina Molecular, Faculdade de Medicina da Universidade de Lisboa, Lisboa, Portugal
    2. Instituto Gulbenkian de Ciência, Oeiras, Portugal
    • CorrespondenceProf. Bruno Silva-Santos, Molecular Immunology Unit, Instituto de Medicina Molecular, Av. Prof. Egas Moniz, 1649-028 Lisboa, Portugal

      Fax: +351-21-798-5142

      e-mail: bssantos@fm.ul.pt

      See accompanying article: http://dx.doi.org/10.1002/eji.201142021

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Abstract

Chemokines are traditionally classified as homeostatic or inflammatory depending on whether they direct leukocyte migration in the absence or presence of inflammatory stimuli. CC chemokine ligand (CCL)25, a ligand for CC chemokine receptor (CCR)9, has mostly been characterized as a homeostatic chemokine that determines the migration pathway of T-cell progenitors within the thymus, and the recruitment of various lymphocyte subsets to the intestinal mucosa. In this issue of the European Journal of Immunology, Costa et al. [Eur. J. Immunol. 2012. 42: 1250–1260] describe a new inflammatory role for CCL25/CCR9 in controlling the migration of a subset of γδ Tcells committed to IL-17 production (γδ17 cells) in a model of allergic pleurisy. Interestingly, the effect of CCL25 was selective for γδ17 cells, as it did not extend to other γδ or αβ T-cell subsets, and resulted in a specific increase of IL-17 (but not IL-4 or IFN-γ) levels in the allergic pleura. In this commentary, I discuss these results in the context of chemokine-mediated recruitment of γδ Tcells to inflammatory sites, and the as yet unclear and controversial role of IL-17 in allergic reactions.

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