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γδ T Cells Mediate a Requisite Portion of a Wound Healing Response Triggered by Cutaneous Poxvirus Infection.
- Source :
-
Viruses (1999-4915) . Mar024, Vol. 16 Issue 3, p425. 30p. - Publication Year :
- 2024
-
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. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 19994915
- Volume :
- 16
- Issue :
- 3
- Database :
- Academic Search Index
- Journal :
- Viruses (1999-4915)
- Publication Type :
- Academic Journal
- Accession number :
- 176333845
- Full Text :
- https://doi.org/10.3390/v16030425