Abstract
Organ transplantation can be considered as replacement therapy for patients with end-stage organ failure. The percent of one-year allograft survival has increased due, among other factors, to a better understanding of the rejection process and new immunosuppressive drugs. Immunosuppressive therapy used in transplantation prevents activation and proliferation of alloreactive T lymphocytes, although not fully preventing chronic rejection. Recognition by recipient T cells of alloantigens expressed by donor tissues initiates immune destruction of allogeneic transplants. However, there is controversy concerning the relative contribution of CD4+ and CD8+ T cells to allograft rejection. Some animal models indicate that there is an absolute requirement for CD4+ T cells in allogeneic rejection, whereas in others CD4-depleted mice reject certain types of allografts. Moreover, there is evidence that CD8+ T cells are more resistant to immunotherapy and tolerance induction protocols. An intense focal infiltration of mainly CD8+CTLA4+ T lymphocytes during kidney rejection has been described in patients. This suggests that CD8+ T cells could escape from immunosuppression and participate in the rejection process. Our group is primarily interested in the immune mechanisms involved in allograft rejection. Thus, we believe that a better understanding of the role of CD8+ T cells in allograft rejection could indicate new targets for immunotherapy in transplantation. Therefore, the objective of the present review was to focus on the role of the CD8+ T cell population in the rejection of allogeneic tissue.
Highlights
The term accessory molecule has been used to describe the activities of CD4 and CD8 when they are unable to bind to the same major histocompatibility complex (MHC) molecule as the T cells (Ts) cell receptor (TCR)
CD8+ T cell helper independence might be related to the avidity of the interaction between T cell receptor (TCR) on these cells and the antigen presented by class I molecules on the antigen-presenting cells (APC)
Deeths et al [4] showed that in vitro a helperindependent phase of the CD8+ T cell response is consistent with the ability of these cells to support their own expansion by producing IL-2 in response to co-stimulation provided by CD28 binding to B7 ligands, leukocyte function accessory-1 molecule (LFA-1) binding to intercellular adhesion
Summary
The term accessory molecule has been used to describe the activities of CD4 and CD8 when they are unable to bind to the same MHC molecule as the TCR. Gilot et al [8] showed that during a heart rejection episode in mice the graft-infiltrating antigen-specific CD8+ T cell population expanded with modulation of surface markers such as CD62L and CD69 besides production of IFN-g.
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More From: Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
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