title: Autophagy in allografts rejection: A new direction?
abstract: Despite the introduction of new and effective immunosuppressive drugs, acute cellular graft rejection is still a major risk for graft survival. Modulating the dosage of immunosuppressive drugs is not a good choice for all patients, new rejection mechanisms discovery are crucial to limit the inflammatory process and preserve the function of the transplant. Autophagy, a fundamental cellular process, can be detected in all subsets of lymphocytes and freshly isolated naive T lymphocytes. It is required for the homeostasis and function of T lymphocytes, which lead to cell survival or cell death depending on the context. T cell receptor (TCR) stimulation and costimulator signals induce strong autophagy, and autophagy deficient T cells leads to rampant apoptosis upon TCR stimulation. Autophagy has been proved to be activated during ischemia-reperfusion (I/R) injury and associated with grafts dysfunction. Furthermore, Autophagy has also emerged as a key mechanism in orchestrating innate and adaptive immune response to self-antigens, which relates with negative selection and Foxp3(+) Treg induction. Although, the role of autophagy in allograft rejection is unknown, current data suggest that autophagy indeed sweeps across both in the graft organs and recipients lymphocytes after transplantation. This review presents the rationale for the hypothesis that targeting the autophagy pathway could be beneficial in promoting graft survival after transplantation.
authors.affiliation: Nuclear Medicine Departments, Central Hospital of Zibo, Zibo, Shandong, 255036, PR China. Electronic address: sunhukui@mail.sdu.edu.cn.
authors.forename: Hukui
authors.initials: H
authors.lastname: Sun
authors.affiliation: Nuclear Medicine Departments, Central Hospital of Zibo, Zibo, Shandong, 255036, PR China.
authors.forename: Dayan
authors.initials: D
authors.lastname: Cheng
authors.affiliation: Nuclear Medicine Departments, Central Hospital of Zibo, Zibo, Shandong, 255036, PR China.
authors.forename: Yuanyuan
authors.initials: Y
authors.lastname: Ma
authors.affiliation: Nuclear Medicine Departments, Central Hospital of Zibo, Zibo, Shandong, 255036, PR China.
authors.forename: Huaiquan
authors.initials: H
authors.lastname: Wang
authors.affiliation: Biomedical Isotope Research Center, School of Medicine, Shandong University, Jinan, Shandong, 250012, PR China.
authors.forename: Ting
authors.initials: T
authors.lastname: Liang
authors.affiliation: Biomedical Isotope Research Center, School of Medicine, Shandong University, Jinan, Shandong, 250012, PR China.
authors.forename: Guihua
authors.initials: G
authors.lastname: Hou
mesh_terms: D064591:Allografts / Q000276:immunology; D000818:Animals; D001324:Autoantigens / Q000276:immunology; D001343:Autophagy / Q000276:immunology*; D006084:Graft Rejection / Q000276:immunology*; D006801:Humans; D007108:Immune Tolerance; D051379:Mice; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D001324:Autoantigens
keywords: Allograft; Autophagy; T lymphocyte; Tolerance; Transplantation