The potential role of intestinal intraepithelial lymphocytes (i-IELs) in the generation of host protective immunity after helminth infection was investigated using the Trichinella spiralis (Owen, 1835)/mouse model. In this study we found a significant rise of TCRyô i-IELs (P < 0.001) concurrent with the jejunal goblet cells (GC) hyperplasia in T. spiralis-infected C57BL mice on day 4 p.i. However, no direct relationship between the kinetics of the increase in TCRy5+ i-IELs and T, spiralis expulsion was observed in infected mice. Taken together, these results implicate that γδ i-IELs probably perform a unique functions related to the regulation of the CiC proliferation accompanying T. spiralis gut infection. As is known, these TCRyS* i-IELs may release mediators or growth factors that in turn influence GC differentiation. With the use of dexamethason (DEX), a potent anti-inflammatory agent which also induces apoplotic ceil death in i-IELs, wc have confirmed that the expulsion of T. spiralis from the mouse gut is accompanied by an inflammatory response. Indeed, the GC are clearly involved in these phenomena, apparently under the regulation by TCRy8+ i-lEL-mediated responses, since DEX abrogated GC proliferation in T. spiralis-infected C57BL mice and subsequently augmented adult worm burden. Our data also show that the rejection of adult worms starts concurrently with a significant increase in TCRaß* and CDS* i-IELs (P < 0.05 and P < 0.01, respectively), namely by day 7 p.i. At the same time, CD4* cells significantly decreased (P < 0.05) in the intestinal epithelium of T. spira/ir-infected, ví uninfected mice. These results may indicate that the TCRaß4 and CDS* i-IELs act as effectors of anti-7’, spiralis defence reactions. The implications of these findings for the potential role of intestinal intraepithélial CD8 and TCRaß' cells in the pathogenesis of the intestinal lesions during T. spiralis gut infection are discussed.