Journal
BLOOD
Volume 114, Issue 13, Pages 2639-2648Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2009-05-220004
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Funding
- Italian Ministry of Health
- Associazione Italiana Ricerca sul Cancro
- Ministero dell'Istruzione
- Universita e Ricerca
- Fondazione Italiana Ricerca sul Cancro
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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. (Blood. 2009; 114: 2639-2648)
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