The CD100 receptor interacts with its plexin B2 ligand to regulate epidermal ?? T cell function.

ABSTRACT: ?? T cells respond rapidly to keratinocyte damage, providing essential contributions to the skin wound healing process. The molecular interactions regulating their response are unknown. Here, we identify a role for interaction of plexin B2 with the CD100 receptor in epithelial repair. In vitro blocking of plexin B2 or CD100 inhibited ?? T cell activation. Furthermore, CD100 deficiency in vivo resulted in delayed repair of cutaneous wounds due to a disrupted ?? T cell response to keratinocyte damage. Ligation of CD100 in ?? T cells induced cellular rounding via signals through ERK kinase and cofilin. Defects in this rounding process were evident in the absence of CD100-mediated signals, thereby providing a mechanistic explanation for the defective wound healing in CD100-deficient animals. The discovery of immune functions for plexin B2 and CD100 provides insight into the complex cell-cell interactions between epithelial resident ?? T cells and the neighboring cells they support.

SUBMITTER: Witherden DA 

PROVIDER: S-EPMC3430606 | biostudies-literature | 2012 Aug

REPOSITORIES: biostudies-literature