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      Mechanism of cellular rejection in transplantation

      other
      Author(s): 1 , 2 ,
      Publication date (Electronic):
      Journal: Pediatric Nephrology (Berlin, Germany)
      Publisher: Springer-Verlag
      Keywords: Allograft, Children, Rejection, T lymphocytes, Transplantation

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          Abstract

          The explosion of new discoveries in the field of immunology has provided new insights into mechanisms that promote an immune response directed against a transplanted organ. Central to the allograft response are T lymphocytes. This review summarizes the current literature on allorecognition, costimulation, memory T cells, T cell migration, and their role in both acute and chronic graft destruction. An in depth understanding of the cellular mechanisms that result in both acute and chronic allograft rejection will provide new strategies and targeted therapeutics capable of inducing long-lasting, allograft-specific tolerance.

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          Most cited references168

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          Two types of murine helper T cell clone. I. Definition according to profiles of lymphokine activities and secreted proteins.

          T R Mosmann, H Cherwinski, M Bond … (1986)
          A panel of antigen-specific mouse helper T cell clones was characterized according to patterns of lymphokine activity production, and two types of T cell were distinguished. Type 1 T helper cells (TH1) produced IL 2, interferon-gamma, GM-CSF, and IL 3 in response to antigen + presenting cells or to Con A, whereas type 2 helper T cells (TH2) produced IL 3, BSF1, and two other activities unique to the TH2 subset, a mast cell growth factor distinct from IL 3 and a T cell growth factor distinct from IL 2. Clones representing each type of T cell were characterized, and the pattern of lymphokine activities was consistent within each set. The secreted proteins induced by Con A were analyzed by biosynthetic labeling and SDS gel electrophoresis, and significant differences were seen between the two groups of T cell line. Both types of T cell grew in response to alternating cycles of antigen stimulation, followed by growth in IL 2-containing medium. Examples of both types of T cell were also specific for or restricted by the I region of the MHC, and the surface marker phenotype of the majority of both types was Ly-1+, Lyt-2-, L3T4+, Both types of helper T cell could provide help for B cells, but the nature of the help differed. TH1 cells were found among examples of T cell clones specific for chicken RBC and mouse alloantigens. TH2 cells were found among clones specific for mouse alloantigens, fowl gamma-globulin, and KLH. The relationship between these two types of T cells and previously described subsets of T helper cells is discussed.
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            T-cell help for cytotoxic T lymphocytes is mediated by CD40-CD40L interactions.

            S. P. Schoenberger, R Toes, E van der Voort … (1998)
            Although in vivo priming of CD8+ cytotoxic T lymphocytes (CTLs) generally requires the participation of CD4+ T-helper lymphocytes, the nature of the 'help' provided to CTLs is unknown. One widely held view is that help for CTLs is mediated by cytokines produced by T-helper cells activated in proximity to the CTL precursor at the surface of an antigen-presenting cell (APC). An alternative theory is that, rather than being directly supplied to the CTL by the helper cell, help is delivered through activation of the APC, which can then prime the CTL directly. CD40 and its ligand, CD40L, may activate the APC to allow CTL priming. CD40L is expressed on the surface of activated CD4+ T-helper cells and is involved in their activation and in the development of their effector functions. Ligation of CD40 on the surface of APCs such as dendritic cells, macrophages and B cells greatly increases their antigen-presentation and co-stimulatory capacity. Here we report that signalling through CD40 can replace CD4+ T-helper cells in priming of helper-dependent CD8+ CTL responses. Blockade of CD40L inhibits CTL priming; this inhibition is overcome by signalling through CD40. CD40-CD40L interactions are therefore vital in the delivery of T-cell help for CTL priming.
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              Interleukin-7 mediates the homeostasis of naïve and memory CD8 T cells in vivo.

              K. S. Schluns, W. Kieper, S. Jameson … (2000)
              The naïve and memory T lymphocyte pools are maintained through poorly understood homeostatic mechanisms that may include signaling via cytokine receptors. We show that interleukin-7 (IL-7) plays multiple roles in regulating homeostasis of CD8+ T cells. We found that IL-7 was required for homeostatic expansion of naïve CD8+ and CD4+ T cells in lymphopenic hosts and for CD8+ T cell survival in normal hosts. In contrast, IL-7 was not necessary for growth of CD8+ T cells in response to a virus infection but was critical for generating T cell memory. Up-regulation of Bcl-2 in the absence of IL-7 signaling was impaired after activation in vivo. Homeostatic proliferation of memory cells was also partially dependent on IL-7. These results point to IL-7 as a pivotal cytokine in T cell homeostasis.
              Article 0 comments Cited 342 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                : eingulli@ucsd.edu
                Journal
                Journal ID (nlm-ta): Pediatr Nephrol
                Title: Pediatric Nephrology (Berlin, Germany)
                Publisher: Springer-Verlag (Berlin/Heidelberg )
                ISSN (Print): 0931-041X
                ISSN (Electronic): 1432-198X
                Publication date (Electronic): 24 October 2008
                Publication date (Print): January 2010
                Volume: 25
                Issue: 1
                Pages: 61-74
                Affiliations
                [1 ]Department of Pediatrics, University of California, San Diego, CA USA
                [2 ]University of California, San Diego, 9500 Gilman Drive MC 0815, La Jolla, CA 92093 USA
                Article
                Publisher ID: 1020
                DOI: 10.1007/s00467-008-1020-x
                PMC ID: 2778785
                PubMed ID: 21476231
                SO-VID: ed14a4c3-3d47-4cfa-aa36-f76beab5126f
                Copyright © © IPNA 2008
                History
                Date received : 20 February 2008
                Date revision received : 31 August 2008
                Date accepted : 9 September 2008
                Categories
                Subject: Educational Review
                Custom metadata
                issue-copyright-statement © IPNA 2010

                ScienceOpen disciplines: Nephrology
                Keywords: children,rejection,t lymphocytes,transplantation,allograft
                Data availability:
                ScienceOpen disciplines: Nephrology
                Keywords: children, rejection, t lymphocytes, transplantation, allograft

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