Search

The epidermis of mouse skin is usually populated by dendritic epidermal T cells (γδDETC) expressing an invariant Vγ5Vδ1+ TCR. In Tcrd-/- mice, skin-resident γδDETC are replaced by αβDETC carrying polyclonal αβ TCRs. Although they exhibit a dendritic morphology, αβDETC were reported to be less functional than genuine γδDETC, likely because their TCR is unable to interact with the original TCR ligands of γδDETC. However, the TCR repertoire of those replacement DETC in Tcrd-/- mice might provide clues for understanding the development and selection of canonical γδDETC. Here, we compare the phenotype and TCR repertoires of wild-type and Tcrd-/- mouse skin T cells. Our data reveal that αβDETC are CD4/CD8 double negative and express an MHC-independent TCR repertoire. Furthermore, we identify a second MHC-independent population of CD103hi CD4/ CD8 double-negative αβ T cells in the dermis of Tcrd-/- mice.

The chemokine receptor CCR7 has a central role in regulating homing and positioning of T cells and DCs to lymph nodes (LNs) and participates in T-cell development and activation. In this study, we addressed the role of CCR7 signaling in TH2 polarization and B-cell activation. We provide evidence that the lack of CCR7 drives the capacity of naive CD4+ T cells to polarize toward TH2 cells. This propensity contributes to a lymph node environment in CCR7-deficent mice characterized by increased expression of IL-4 and increased frequency of TH2 cells. We show that elevated IL-4 levels lead to B-cell activation characterized by up-regulated expression of MHC class II, CD23 and CD86. Activated B cells are in turn highly efficient in presenting antigen to CD4+ T cells and thus potentially contribute to the TH2 microenvironment. Taken together, our results support the idea of a CCR7-dependent patterning of TH2 responses, with absent CCR7 signaling favoring TH2 polarization, dislocation of T helper cells into the B-cell follicles and, as a consequence, B-cell activation.