Purpose of review: Ischemia and reperfusion injuries occur in multiple clinical settings and contribute to organ dysfunction/failures. Despite the innate inflammatory immune nature, T cells that are critically involved in the pathogenesis of ischemia reperfusion injury (IRI), include not only CD4+ T cells, but also CD8+ and γδT cells. This review focuses on questions of how putative Ag-specific T cells are involved, which include whether they function in an Ag-dependent manner; how they function, cytokine-mediated or costimulatory molecule-mediated mechanisms; and whether different T-cell subsets, Th1, Th17, regulatory T cell (Treg), are all involved and play distinctive roles?
Recent findings: Specific T-cell populations, such as effector memory CD4 T cells, promote inflammatory immune activation by ischemia reperfusion independent of their adaptive properties, that is Ag-independently. They function by secreting cytokines and expressing costimulatory molecules to either promote or inhibit innate immune activation, or facilitate tissue repair/homeostasis, as exemplified by Th1, Th17 or Th2, Treg cells, respectively.
Summary: T-cell-targeted therapies need to be refined with strategies to maximally eliminate the proinflammatory but spare the anti-inflammatory/immune regulatory properties of T cells, for future clinical application to ameliorate IRI.
aDumont-UCLA Transplant Center, Division of Liver and Pancreas Transplantation, Department of Surgery, David Geffen School of Medicine at University of California-Los Angeles, Los Angeles, California, USA
bLiver Transplantation Center, Department of Liver Surgery, First Affiliated Hospital of Nanjing Medical University Nanjing, Jiangsu Province, China
Correspondence to Yuan Zhai, MD, PhD, Dumont-UCLA Transplant Center 77-120 CHS, 10833 Le Conte Ave, Los Angeles, CA 90095, USA. Tel: +1 310 825 9426; fax: +1 310 267 2367; e-mail: email@example.com