PDF(Pubmed)
Abstract：
Infection at barrier sites, e.g., skin, activates local immune defenses that limit pathogen spread, while preserving tissue integrity. Phenotypically distinct γδ T cell populations reside in skin, where they shape immunity to cutaneous infection prior to onset of an adaptive immune response by conventional αβ CD4+ (TCD4+) and CD8+ (TCD8+) T cells. To examine the mechanisms used by γδ T cells to control cutaneous virus replication and tissue pathology, we examined γδ T cells after infection with vaccinia virus (VACV). Resident γδ T cells expanded and combined with recruited γδ T cells to control pathology after VACV infection. However, γδ T cells did not play a role in control of local virus replication or blockade of systemic virus spread. We identified a unique wound healing signature that has features common to, but also features that antagonize, the sterile cutaneous wound healing response. Tissue repair generally occurs after clearance of a pathogen, but viral wound healing started prior to the peak of virus replication in the skin. γδ T cells contributed to wound healing through induction of multiple cytokines/growth factors required for efficient wound closure. Therefore, γδ T cells modulate the wound healing response following cutaneous virus infection, maintaining skin barrier function to prevent secondary bacterial infection.
摘要：
屏障部位感染,例如，皮肤,激活局部免疫防御，限制病原体传播，同时保持组织的完整性。表型不同的γδT细胞群存在于皮肤中，在常规αβCD4（TCD4）和CD8（TCD8）T细胞发生适应性免疫反应之前，它们会形成对皮肤感染的免疫力。为了检查γδT细胞控制皮肤病毒复制和组织病理学的机制，我们检测了痘苗病毒（VACV）感染后的γδT细胞。VACV感染后，居民γδT细胞扩增并与募集的γδT细胞结合以控制病理。然而,γδT细胞在控制局部病毒复制或阻断系统病毒传播中不起作用。我们发现了一种独特的伤口愈合特征，而且还有对抗的特征，无菌皮肤伤口愈合反应。组织修复通常发生在病原体清除后，但是病毒伤口愈合在皮肤病毒复制高峰之前就开始了。γδT细胞通过诱导有效伤口闭合所需的多种细胞因子/生长因子来促进伤口愈合。因此,γδT细胞调节皮肤病毒感染后的伤口愈合反应，维持皮肤屏障功能，防止继发细菌感染。
