Gliadin-mediated proliferation and innate immune activation in celiac disease are due to alterations in vesicular trafficking.

ABSTRACT:

Background and objectives

Damage to intestinal mucosa in celiac disease (CD) is mediated both by inflammation due to adaptive and innate immune responses, with IL-15 as a major mediator of the innate immune response, and by proliferation of crypt enterocytes as an early alteration of CD mucosa causing crypts hyperplasia. We have previously shown that gliadin peptide P31-43 induces proliferation of cell lines and celiac enterocytes by delaying degradation of the active epidermal growth factor receptor (EGFR) due to delayed maturation of endocytic vesicles. IL-15 is increased in the intestine of patients affected by CD and has pleiotropic activity that ultimately results in immunoregulatory cross-talk between cells belonging to the innate and adaptive branches of the immune response.

SUBMITTER: Barone MV 

PROVIDER: S-EPMC3045409 | biostudies-literature | 2011 Feb

REPOSITORIES: biostudies-literature