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 Blood, 24 September 2009, Vol. 114, No. 13, pp. 2639-2648.
Prepublished online as a Blood First Edition Paper on July 30, 2009; DOI 10.1182/blood-2009-05-220004.

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IMMUNOBIOLOGY

Mast cells counteract regulatory T-cell suppression through interleukin-6 and OX40/OX40L axis toward Th17-cell differentiation

Silvia Piconese1,*, Giorgia Gri2,*, Claudio Tripodo3, Silvia Musio4, Andrea Gorzanelli1, Barbara Frossi2, Rosetta Pedotti4, Carlo E. Pucillo2, and Mario P. Colombo1

1 Molecular Immunology Unit, Department of Experimental Oncology, Fondazione Istituto di Ricovero e Cura a Carattere Scientifico Istituto Nazionale dei Tumori, Milan; 2 Department of Biomedical Science and Technology, University of Udine, Udine; 3 Department of Human Pathology, University of Palermo, Palermo; and 4 Immunology and Muscular Pathology Unit, Neurologic Institute Foundation Carlo Besta, Milan, Italy

The development of inflammatory diseases implies inactivation of regulatory T (Treg) cells through mechanisms that still are largely unknown. Here we showed that mast cells (MCs), an early source of inflammatory mediators, are able to counteract Treg inhibition over effector T cells. To gain insight into the molecules involved in their interplay, we set up an in vitro system in which all 3 cellular components were put in contact. Reversal of Treg suppression required T cell–derived interleukin-6 (IL-6) and the OX40/OX40L axis. In the presence of activated MCs, concomitant abundance of IL-6 and paucity of Th1/Th2 cytokines skewed Tregs and effector T cells into IL-17–producing T cells (Th17). In vivo analysis of lymph nodes hosting T-cell priming in experimental autoimmune encephalomyelitis revealed activated MCs, Tregs, and Th17 cells displaying tight spatial interactions, further supporting the occurrence of an MC-mediated inhibition of Treg suppression in the establishment of Th17-mediated inflammatory responses.


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