The role of γδ T cells in the regulation of neutrophil-mediated tissue damage after thermal injury

Abstract

Thermal injury induces an inflammatory response that contributes to the development of secondary tissue damage. Neutrophil recruitment and activation are in part responsible for this tissue damage. Although gammadelta T cells have been shown to regulate the inflammatory responses in tissues that are prone to neutrophil-mediated injury post-burn, their role in the induction of secondary tissue injury post-burn remains unknown. To study this, gammadelta T cell-deficient (gammadelta TCR-/-) and wild-type (WT) mice were subjected to thermal injury or sham procedure, and tissue samples were isolated 1-24 h thereafter. Burn injury induced neutrophil accumulation in the lung and small intestines of WT mice at 1-3 h post-injury. No such increase in neutrophil tissue content was observed in gammadelta TCR-/- mice. An increase in tissue wet/dry weight ratios was also observed in these organs at 3 h post-burn in WT but not in gammadelta TCR-/- mice. A parallel increase in plasma and small intestine levels of the chemokines macrophage-inflammatory protein-1beta (chemokine ligand 4) and keratinocyte-derived chemokine (CXC chemokine ligand 1) were observed in injured WT mice but not in injured gammadelta TCR-/- mice. Increased activation (CD120b expression) of the circulating gammadelta T cell population was also observed at 3 h post-burn in WT mice. These results indicate the gammadelta T cells, through the production of chemokines, play a central role in the initiation of neutrophil-mediated tissue damage post-burn.

Dermal-Resident versus Recruited γδ T Cell Response to Cutaneous Vaccinia Virus Infection

“…5D, 5E). The ability of pThy-derived dermal gd T cells to recruit inflammatory cells, such as neutrophils, is likely due to their production of IL-17 (16,20,42), and recruitment of neutrophils by gd T cells directly results in increased tissue damage (43). We demonstrated increased necrosis and cellularity of infected ears 3 d after VV infection, indicating that the resident IL-17 + gd T cells are early responders to viral infection.…”

Heat-shock protein 70 expression in the seminal plasma of patients with chronic bacterial prostatitis and chronic prostatitis/chronic pelvic pain syndrome

“…[24][25][26] It has been well demonstrated that HSP70, also called stress protein, may participate in the cellular response to hyperthermia, ischemic injury, infection and autoimmune diseases. [27][28][29][30] The protein serves as a chaperone molecule for various intracellular proteins and may alter their functional characteristics. The induction of HSP70 expression by bacterial infection has a role in the cellular response to injury.…”

Adipose tissues as an ancestral immune organ: Site‐specific change in obesity

“…The role of cd cells has not been yet totally elucidated but beside their protective immunity against infections and tumors, immunoregulation is an emerging paradigm of their function. For instance, in liver and mucosal surfaces, these T cells have regulatory roles such as initiating or inhibiting inflammation [15,17,26] and they contribute to macrophage homeostasis [13,27]. Whether they play such roles in adipose tissues remains to be elucidated.…”