Scaffolding protein Gab1 regulates myeloid dendritic cell migration in allergic asthma.

摘要: Asthma is a common allergic disorder involving complex interplay among multiple genetic and environmental factors. Recent studies identified variants of human GAB1 as novel asthma susceptibility factor. However, the functions Gab1 in lung remain largely unexplored. In this study, we first observed an elevation level peripheral blood mononuclear cells from asthmatic patients during acute exacerbation compared with convalescence. Mice selectively disrupted myeloid dendritic (mDCs) considerably attenuated inflammation experimental models asthma. Further investigations revealed prominent reduction CCL19-mediated migration Gab1-deficient mDCs to draining lymph nodes subsequent impairment Th2-driven adaptive activation. Mechanistically, essential component CCL19/CCR7 chemokine axis that regulates mDC responses. Together, these findings provide evidence for roles lung, giving us deeper understanding pathogenesis.