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Commentary |
Fondazione Istituto Di Ricovero e Cura a Carattere Scientifico "Istituto Nazionale dei Tumori," Milan, Italy
* To whom correspondence should be addressed. E-mail: mario.colombo{at}istitutotumori.mi.it.
| Abstract |
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Gounaris and colleagues describe a previously unrecognized cross-talk between mast cells and Treg in colon adenomatous polyposis (Gounaris et al., Cancer Res 2009;69:5790–7). Adoptively transferred Treg suppress the focal mastocytosis that fosters tumor initiation and progression. In contrast, endogenous Treg, which abundantly infiltrate polyps, show proinflammatory activity under unknown microenvironmental cues that promote mast cell differentiation and expansion. Compartmentalized Treg plasticity seems to be a key factor in establishing the optimal milieu for cancer development in the intestines. Treg partnership with mast cells recapitulates the complexity of innate-adaptive networks characterizing gut inflammation and represents a novel target for cancer immunotherapy. [Cancer Res 2009;69(14):5619–22]
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