Among their many crucial roles in mediating the interactions of cells with other cells and with their environment, integrins allow lymphocytes to adhere to the endothelium, and to migrate across it into infected tissues. The b7 integrins a4b7 and aEb7 have been implicated in trafficking of lymphocytes to the epithelial lining of the intestine and in the retention of lymphocytes at this site. Earlier work suggested that these integrins were essential for controlling infections by diarrhea-inducing rotaviruses, which proliferate in the intestinal mucosa, but the current report by Kuklin and colleagues tells a different tale. These authors show that in mice lacking b7 integrins, immune responses to rotavirus infection are indeed abnormal. In particular, B cell–mediated secretion of antiviral IgA is lacking in these mutant animals, consistent with other work showing that that B-cell trafficking to gut-associated lymphoid tissue depends on b7 integrins. In addition, CD8+ T cells from b7-deficient mice reach the intestinal epithelium in smaller numbers following rotavirus infection, relative to similarly infected wild-type animals. Nevertheless, some CD8+ T cells do reach the site of infection, by means of still-uncharacterized adhesive interactions, and these cells are sufficient to clear the virus efficiently from the gut. Indeed, the infection is resolved equally quickly in wild-type and mutant animals.
Journal of Clinical Investigation