Scald Injury-Induced T Cell Dysfunction Can Be Mitigated by Gr1⁺ Cell Depletion and Blockage of CD47/CD172a Signaling.

ABSTRACT: Infection is a common and severe complication of burn injury: Sepsis accounts for 47% of postburn mortality. Burn-induced T cell suppression likely contributes to the increased infection susceptibility in burn patients. However, little is known about the kinetics of T cell dysfunction after burn and its underlying mechanisms. In this study, we show in a murine scald injury model that T cell activation of both CD4⁺ and CD8⁺ T cells as well as T cell cytokine production is suppressed acutely and persistently for at least 11 days after burn injury. Purified T cells from scald-injured mice exhibit normal T cell functions, indicating an extrinsically mediated defect. We further show that T cell dysfunction after burn appears to be cell-to-cell contact dependent and can be

SUBMITTER: Beckmann N 

PROVIDER: S-EPMC7232553 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature