CD4+ T cell‐mediated rejection of major histocompatibility complex class I‐disparate grafts: A role for alloantibody

@article{Morton1993CD4TC,
  title={CD4+ T cell‐mediated rejection of major histocompatibility complex class I‐disparate grafts: A role for alloantibody},
  author={A. Lawrie Morton and Eric B. Bell and Eleanor M. Bolton and Hilary Marshall and Chris Roadknight and Mark McDonagh and J Andrew Bradley},
  journal={European Journal of Immunology},
  year={1993},
  volume={23}
}
Experimental studies of the T cell requirement for rejection of class I major histocompatibility complex (MHC)‐disparate grafts have generated controversy over both the autonomy of CD8+ T cells and the mechanism whereby CD4+ T cells are able to independently mediate rejection. In this study of rejection of RT1Aa class I MHC‐disparate rat cardiac and skin allografts by high‐responder PVG RT1u recipients, we show that elimination of CD8+ T cells [by anti‐CD8 monoclonal antibody (mAb… 
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CD4 T cells can reject major histocompatibility complex class I‐incompatible skin grafts
TLDR
It is surmised that for CD4 T cells to reject an MHC class I‐incompatible graft it is necessary that an appropriate allogeneic peptide is processed and presented in the context of recipient MHCclass II.
Indirect T cell allorecognition and alloantibody-mediated rejection of MHC class I-disparate heart grafts.
TLDR
Results suggest that both soluble MHC class I and allopeptides prime CD4 T cells by the indirect pathway, but that soluble class I is a more effective immunogen for humoral alloimmunity because its tertiary protein structure provides B cell epitopes.
Abrogation of Antibody-Mediated Allograft Rejection by Regulatory CD4 T Cells with Indirect Allospecificity1
TLDR
It is demonstrated that anti-CD4 plus donor-specific transfusion treatment results in the development of CD4 regulatory T cells that recognize alloantigen-specific B cell compartment that persists after T cell help is made available and act in an Ag-specific manner to preventalloantibody-mediated rejection.
Persisting alloantigen prevents primed CD45RC − CD4 T cells from inducing allograft rejection: implications for immunological memory
TLDR
It is shown that an allogeneic blood transfusion primes (not tolerizes) alloreactive CD4 T’cells and that residual DST‐derived alloantigen can block the action of specifically primed “memory” CD4T’s, which have implications for understanding immunological memory.
Decreased anti‐donor major histocompatibility complex class I and increased class II alloantibody response in allograft tolerance in adult rats
TLDR
It is suggested that the absence of anti‐class I alloantibodies combined with preserved and/or increased anti‐ class II production plays a major role in graft tolerance in this model of heart allografts.
Rejection of grafts with no H-2 disparity in TAP1 mutant mice: CD4 T cells are important effector cells and self H-2b class I molecules are target.
Acute rejection of vascular heart allografts by perforin‐deficient mice
TLDR
Data indicate that perforin is not essential in the cell‐mediated acute rejection of a fully mismatched heart allograft, and Perforin‐dependent effector mechanisms appeared to be limiting in the T cellmediated rejection of heart allogsrafts differing only at a single major histocompatibility complex class I antigen.
Alloantibody and intragraft cellular response to MHC class I-disparate kidney allografts in recipients tolerized by donor-specific transfusion and cyclosporine.
TLDR
It is shown that PVG.RT1u recipients can be rendered permanently and specifically tolerant to R8 kidney allografts by administration of four weekly donor-specific transfusions (DST) combined with a 7-day course of cyclosporine given with the first DST.
The role of CD8 and CD4 T cells in intestinal allograft rejection: a comparison of monoclonal antibody-treated and knockout mice.
TLDR
These results demonstrate that the inhibition of intestinal allograft rejection associated with mAb treatment is not attributable solely to depletion of CD8 or CD4 T cells and suggest that at least some depleting mAbs mediate their protective effect on allografted rejection via an alternative mechanism such as the induction of a regulatory cell population(s).
Dendritic cells internalise and re‐present conformationally intact soluble MHC class I alloantigen for generation of alloantibody
TLDR
A novel alloantigen recognition pathway whereby soluble MHC class I alloantsigen released from an allograft may be taken up by recipient DC and presented in an intact unprocessed form to B cells for the generation of analloantibody response.
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References

SHOWING 1-10 OF 82 REFERENCES
Cellular basis of skin allograft rejection across a class I major histocompatibility barrier in mice depleted of CD8+ T cells in vivo
TLDR
It is observed that the additional alloantigens coexpressed on MHC class I disparate grafts that triggered graft rejection in CD8-depleted mice could be MHC-linked or not and they functioned in these rejection responses to activate third party specific CD4+ T helper (Th) cells to provide helper signals for the generation of CD8+ anti-CD8 resistant CTL effector cells.
Mechanism of the rejection of major histocompatibility complex class I- disparate murine skin grafts: rejection can be mediated by CD4+ cells activated by allo-class I + II antigen in CD8+ cell-depleted hosts
TLDR
It was immunohistochemically revealed that under that condition, a large number of CD4+ cells infiltrated into the epithelial tissue of these long-surviving class I grafts, which were going to be rejected 2-5 d after the transplantation of a second graft with MHC class I + II difference.
T cell requirements for the rejection of renal allografts bearing an isolated class I MHC disparity
TLDR
CD8+ cells in general and CD8+ cytotoxic effector cells in particular are unnecessary for the rapid rejection of RT1Aa class I disparate kidney grafts by high responder RT1u recipients by implication, CD4+ T cells alone are sufficient to cause prompt rejection of such grafts and they may do so by providing T cell help for the generation of alloantibody.
Allograft rejection in athymic nude rats by transferred T cell subsets. II. The response of naive CD4+ and CD8+ thoracic duct lymphocytes to an isolated MHC class I disparity.
TLDR
It is concluded that CD4+ T cells were required for rejection of both class I and class II differences, and sequential transfer in the reverse order apparently induced tolerance in theCD4+ population.
Heterogenous graft rejection pathways in class I major histocompatibility complex-disparate combinations and their differential susceptibility to immunomodulation induced by intravenous presensitization with relevant alloantigens
TLDR
The results indicate that the graft rejection in class I-disparate combinations is induced by CD8+ CTL-involved and -independent pathways that are resistant and susceptible to DSP, respectively; and the suppression of graft rejection requires an additional treatment for reducing DSP-resistant CTL responses.
Renal allograft rejection in CD4+ T cell-reconstituted athymic nude rats. The origin of CD4+ and CD8+ graft-infiltrating cells.
TLDR
To establish the provenance of these CD8+ cells infiltrating rejecting kidney allografts, nude recipients were injected with CD4+ T cells from the PVG-RT7b congenic strain bearing an allotypic variant of the leukocyte-common antigen.
Phenotype, specificity, and function of T cell subsets and T cell interactions involved in skin allograft rejection
TLDR
It was found that skin allograft rejection in nude mice required the transfer of immunocompetent T cells and that such reconstitution did not itself stimulate the appearance of T cells derived from the nude host.
Cellular requirements for renal allograft rejection in the athymic nude rat
TLDR
It is suggested that injected CD4+ cells may cause renal allograft rejection by the recruitment of extrathymically derived, widely alloreactive cells into the kidney in this model of graft rejection.
Differential involvement of CD4+ cells in mediating skin graft rejection against different amounts of transgenic H-2K(b) antigen
TLDR
Findings indicate that a quantitative difference of class I antigen caused differential activation of CD4+ cells under conditions in which CD8+ cells were blocked by administration of anti-CD8 monoclonal antibody.
CD4-CD8- T cell receptor alpha beta T cells: generation of an in vitro major histocompatibility complex class I specific cytotoxic T lymphocyte response and allogeneic tumor rejection
TLDR
The finding that adoptive transfer of CD4 and CD8-depleted MLTC spleen cells, obtained from anti-Lyt-2.2 (CD8) mAb-treated B6 mice that had rejected BALB RL male 1, resulted in rejection of BALBRL male 1 inoculated into B6 nu/nu mice confirmed the above notion.
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