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Mast Cell Degranulation Breaks Peripheral Tolerance

2009; Elsevier BV; Volume: 9; Issue: 10 Linguagem: Inglês

10.1111/j.1600-6143.2009.02755.x

1600-6143

Victor C. de Vries, Anna Wasiuk, Kathryn A. Bennett, Micah J. Benson, Raúl Elgueta, Thomas J. Waldschmidt, Randolph J. Noelle,

Food Allergy and Anaphylaxis Research

Mast cells (MC) have been shown to mediate regulatory T-cell (Treg)-dependent, peripheral allograft tolerance in both skin and cardiac transplants. Furthermore, Treg have been implicated in mitigating IgE-mediated MC degranulation, establishing a dynamic, reciprocal relationship between MC and Treg in controlling inflammation. In an allograft tolerance model, it is now shown that intragraft or systemic MC degranulation results in the transient loss of Treg suppressor activities with the acute, T-cell dependent rejection of established, tolerant allografts. Upon degranulation, MC mediators can be found in the skin, Treg rapidly leave the graft, MC accumulate in the regional lymph node and the Treg are impaired in the expression of suppressor molecules. Such a dramatic reversal of Treg function and tissue distribution by MC degranulation underscores how allergy may causes the transient breakdown of peripheral tolerance and episodes of acute T-cell inflammation.