Gamma Delta T Cells Regulate Wound Myeloid CELL Activity After Burn

Rani, Meenakshi*; Zhang, Qiong*; Schwacha, Martin G.*†

Shock:
doi: 10.1097/SHK.0000000000000176
Basic Science Aspects
Editor's Choice
Abstract

ABSTRACT: Major burns induce immune complications, which are associated with myeloid cell activation by ill-defined mechanisms. Although γδ T cells have been shown to be important in postinjury inflammation and wound healing, their role in the regulation of myeloid cells remains unknown. To study this, wild-type (WT) and γδ T cell–deficient (δTCR-/-) mice were subjected to major burn (25% total body surface area, third degree) or sham treatment. At 3 days thereafter, skin samples were assayed for cytokine content or used to isolate single cells that were used for myeloid cell characterization by flow cytometry. The number of CD11b+ myeloid cells increased by approximately 75% in the wound skin of WT mice. This influx was caused by increased myeloid-derived suppressor cells (CD11b+ GR1+) whose numbers increased 19-fold compared with those of sham skin. In contrast, macrophage (MØ; CD11b+ F4/80+) numbers decreased by approximately 50% after burn. In δTCR-/- mice, burn increased the myeloid cell numbers approximately 5-fold. The increase in myeloid cells at the injury site of δTCR-/- mice was caused by both a myeloid-derived suppressor cell (50-fold) and a MØ (2-fold) influx. Burn increased skin cytokine levels for a number of prototypic inflammatory cytokines (interleukin 1β, interleukin 6, tumor necrosis factor-α, macrophage inflammatory protein [MIP] 1β, etc). Tumor necrosis factor-α, MIP-1α, and MIP-1β levels were further elevated (2- to 3-fold) in the injured skin of δTCR-/- mice compared with those of WT mice. In conclusion, these data show that γδ T cells regulate myeloid cell infiltration of the wound site and act to quell inflammation, thereby promoting the transition to the proliferative phase of wound healing.

Author Information

*Department of Surgery, The University of Texas Health Science Center, San Antonio; and US Army Institute of Surgical Research, Fort Sam Houston, Texas

Received 5 Nov 2013; first review completed 20 Nov 2013; accepted in final form 12 Mar 2014

Address reprint requests to Martin G. Schwacha, PhD, University of Texas Health Science Center at San Antonio, Department of Surgery Mail Code 7740, 7703 Floyd Curl Dr, San Antonio TX 78229-3900. E-mail: schwacha@uthscsa.edu.

This study was supported by the National Institutes of Health (grant no. GM079122).

The authors have no relevant conflicts of interest.

© 2014 by the Shock Society