Lack of gamma delta T cells ameliorates inflammatory response after acute intestinal ischemia reperfusion in mice

T-cells have been demonstrated to modulate ischemia-reperfusion injury (IRI) in the kidney, lung, liver, and intestine. Whereas most T-cell subpopulations contribute primarily to the antigen-specific effector and memory phases of immunity, gamma delta-T-cells combine adaptive features with rapid, innate-like responses that can place them in the initiation phase of immune reactions. Therefore, we aimed to clarify the role of gamma delta-T-cells in intestinal IRI. Adult wild-type (WT) and gamma delta-T-cell-deficient mice were subjected to acute intestinal IRI. Gene expression of pro-inflammatory cytokines and influx of leukocyte subpopulations in the gut were assessed by qPCR and flow cytometry. Serum transaminases were measured as an indicator of distant organ IRI. Intestinal IRI led to increased influx of neutrophils, pro-inflammatory cytokine expression and LDH/ALT/AST elevation. Selective deficiency of gamma delta-T-cells significantly decreased pro-inflammatory cytokine levels and neutrophil infiltration in the gut following IRI compared to controls. Furthermore, gamma delta-T-cell deficiency resulted in decreased LDH and transaminases levels in sera, indicating amelioration of distant organ injury. Increasing evidence demonstrates a key role of T-cell subpopulations in IRI. We demonstrate that gamma delta-T-cell deficiency ameliorated pro-inflammatory cytokine production, neutrophil recruitment and distant organ injury. Thus, gamma delta-T-cells may be considered as mediators contributing to the inflammatory response in the acute phase of intestinal IRI.

Automated summary

Research has shown that gamma delta-T cells play a significant role in intestinal ischemia-reperfusion injury, and their deficiency can alleviate pro-inflammatory cytokine production, neutrophil infiltration, and distant organ injury.