The CD100 receptor interacts with its plexin B2 ligand to regulate epidermal γδ T cell function.
Immunity
; 37(2): 314-25, 2012 Aug 24.
Article
em En
| MEDLINE
| ID: mdl-22902232
ABSTRACT
γδ 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 γδ T cell activation. Furthermore, CD100 deficiency in vivo resulted in delayed repair of cutaneous wounds due to a disrupted γδ T cell response to keratinocyte damage. Ligation of CD100 in γδ 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 γδ T cells and the neighboring cells they support.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Linfócitos T
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Antígenos CD
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Células de Langerhans
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Receptores de Antígenos de Linfócitos T gama-delta
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Semaforinas
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Proteínas do Tecido Nervoso
Tipo de estudo:
Prognostic_studies
Limite:
Animals
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Humans
Idioma:
En
Ano de publicação:
2012
Tipo de documento:
Article