Enteric infection acts as an adjuvant for the response to a model food antigen

Oral administration of soluble protein Ags typically induces Ag-specific sy stemic nonresponsiveness, However, we have found that feeding a model food protein, OVA, to helminth-infected mice primes for a systemic OVA-specific Th2 response. In this report we show that, in addition to creating a Th2-pr iming cytokine environment, helminth infection up-regulates costimulatory m olecule expression on mucosal, but not peripheral, APCs, To examine the con sequences of mucosal infection for the T cell response to orally administer ed Ag, we adoptively transferred transgenic, OVA-specific, T cells into nor mal mice. We found that helminth infection enhances the expansion and survi val of transgenic T cells induced by Ag feeding. Transfer of 5,6-carboxyflu orescein diacetate succinimidyl ester-labeled donor,cells showed that T cel l proliferation in response to Ag feeding takes place primarily. in the mes enteric lymph nodes. Upon subsequent peripheral exposure to Ag in adjuvant, the proliferative capacity of the transferred transgenic T cells was reduc ed in noninfected mice that had been fed OVA, Helminth infection abrogated this reduction in proliferative capacity. Our data suggests that enteric in fection can act as an adjuvant for the response to dietary Ags and has impl ications for allergic responses to food and the efficacy of oral vaccinatio n.