Vps33B in Dendritic Cells Regulates House Dust Mite-Induced Allergic Lung Inflammation

Dendritic cells (DCs) are the most specialized APCs that play a critical role in driving Th2 differentiation, but the mechanism is not fully understood. Here we show that vacuolar protein sorting 33B (Vps33B) plays an important role in this process. Mice with Vps33b-specific deletion in DCs, but not in macrophages or T cells, were more susceptible to Th2-mediated allergic lung inflammation than wild-type mice. Deletion of Vps33B in DCs led to enhanced CD4(+) T cell proliferation and Th2 differentiation. Moreover, Vps33B specifically restrained reactive oxygen species production in conventional DC1s to inhibit Th2 responses in vitro, whereas Vps33B in monocyte-derived DCs and conventional DC2s was dispensable for Th2 development in asthma pathogenesis. Taken together, our results identify Vps33B as an important molecule that mediates the cross-talk between DCs and CD4(+) T cells to further regulate allergic asthma pathogenesis.

Automated summary

This study shows that the absence of Vps33B in DCs exacerbates Th2-mediated allergic lung inflammation, revealing the regulatory role of cross-talk between DCs and CD4(+) T cells in the pathogenesis of allergic asthma.