Department of Surgery, Washington University School of Medicine, St. Louis, MO, USA.
Expert Rev Clin Immunol. 2012 Sep;8(7):663-72. doi: 10.1586/eci.12.58.
Despite progress in the field of organ transplantation for improvement in graft survival and function, long-term graft function is still limited by the development of chronic allograft rejection. Various immune-mediated and nonimmune-mediated processes have been postulated in the pathogenesis of chronic rejection. In this review, the authors discuss the important role of alloimmune responses to donor-specific antigens and autoimmune responses to tissue restricted self-antigens in the immunopathogenesis of chronic rejection following solid organ transplantation. In particular, the authors discuss the role of induction of Th17-type autoimmune responses and the crosstalk between autoimmune and alloimmune responses. These self-perpetuate each other leading to activation of profibrotic and proinflammatory cascades that ultimately result in the development of chronic rejection.
尽管在器官移植领域取得了进展,以改善移植物的存活和功能,但长期移植物功能仍然受到慢性同种异体排斥反应的限制。在慢性排斥反应的发病机制中,已经提出了各种免疫介导和非免疫介导的过程。在这篇综述中,作者讨论了同种异体反应对供体特异性抗原和自身免疫反应对组织特异性自身抗原的重要作用在实体器官移植后慢性排斥反应的免疫发病机制中的作用。特别是,作者讨论了诱导 Th17 型自身免疫反应和自身免疫与同种异体免疫反应之间的串扰的作用。这些相互促进,导致致纤维化和促炎级联反应的激活,最终导致慢性排斥反应的发生。