Role of Lymphokine in Islet Allograft Rejection

Lm, Hao; Wang, Y; Rg, Gill; Fg, La Rosa; Dw, Talmage; Lafferty, Kevin J.

doi:10.1097/00007890-199003000-00025

Cited by 34 publications

(8 citation statements)

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“…This fact was borne out by the finding that relatively few heavily divided memory cells were detected 25 days after transplantation. Inflammation, and the production of IFN-␥, would up-regulate MHC class I expression by the islets rendering them more susceptible to killing by activated, directly alloreactive cytotoxic CD8 ϩ T cells (33). In addition, IL-1 is a potent modulator of insulin secretion and at high concentrations is cytotoxic to ␤-cells (34,35).…”

Section: Figure 4 Detection Of Memory/effector Cd8mentioning

confidence: 99%

Differential Susceptibility of Heart, Skin, and Islet Allografts to T Cell-Mediated Rejection

Jones

Turvey

Maurik

et al. 2001

The Journal of Immunology

164

135

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Although it is widely accepted that there is a hierarchy in the susceptibility of different allografts to rejection, the mechanisms responsible are unknown. We show that the increased susceptibility of H-2Kb+ skin and islet allografts to rejection is not based on their ability to activate more H-2Kb-specific T cells in vivo; heart allografts stimulate the activation and proliferation of many more H-2Kb-specific T cells than either skin or islet allografts. Rejection of all three types of graft generate memory cells by 25 days posttransplant. These data provide evidence that neither tissue-specific Ags nor, surprisingly, the number of APCs carried in the graft dictate their susceptibility to T cell-mediated rejection and suggest that the graft microenvironment and size may play a more important role in determining the susceptibility of an allograft to rejection and resistance to tolerance induction.

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Section: Figure 4 Detection Of Memory/effector Cd8mentioning

confidence: 99%

Differential Susceptibility of Heart, Skin, and Islet Allografts to T Cell-Mediated Rejection

Jones

Turvey

Maurik

et al. 2001

The Journal of Immunology

164

135

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“…The role of cell-mediated immunity in the rejection of islet allografts has been well studied, and considerable progress has been made in identifying the cellular requirements for the induction of this response (1)(2)(3)(4)(5). Most studies indicate that optimal islet allograft immunity requires both CD4 and CD8 T-cells.…”

mentioning

confidence: 99%

The Degree of Phylogenetic Disparity of Islet Grafts Dictates the Reliance on Indirect CD4 T-Cell Antigen Recognition for Rejection

Rayat

Johnson²,

Beilke³

et al. 2003

Diabetes

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1Cellular xenograft rejection involves a pronounced contribution of CD4 T-cells recognizing antigens in association with recipient MHC class II molecules. However, the requirement for such "indirect" antigen recognition for acute islet xenograft is not clear, especially as a function of the phylogenetic disparity between the donor and recipient species. In vitro studies show that C57BL/6 (B6) mouse T-cells respond directly to either allogeneic BALB/c or phylogenetically related xenogeneic WF rat stimulator cells while having undetectable responses to phylogenetically disparate porcine stimulator cells. Although all types of grafts rejected acutely in wild-type mice, this response demonstrated markedly differing dependence on host MHC class II antigen presentation, depending on the donor species. While BALB/c islet allografts were acutely rejected in B6 MHC class II-deficient (C2D) recipients, WF rat xenografts demonstrated marked prolongation in C2D hosts relative to wild-type recipients. Interestingly, neonatal porcine islet (NPI) xenografts uniformly survived long term (>100 days) in untreated C2D hosts despite transfer of wild-type CD4 T-cells, demonstrating that survival in C2D recipients was not secondary to a lack of CD4 T-cells seen in such mice. Taken together, these results show a marked hierarchy in the requirement for host MHC class II-restricted indirect pathway in the rejection of pancreatic islet grafts. Thus, while cellular rejection of porcine xenografts is generally quite vigorous, this pathway is relatively finite, displaying a major reliance on host MHC class II-dependent antigen presentation for acute rejection.

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“…For example, donor MHC class I is necessary for islet (31) but not heart (32) rejection in the same donor-recipient combination. Also, CD4 T cells are required for islet but not fetal pancreas rejection (33). Thus, the tissue or organ type used for transplantation represents an important variable in dictating the cellular requirements for rejection.…”

mentioning

confidence: 99%

CD4 T cell–mediated cardiac allograft rejection requires donor but not host MHC class II

Pietra¹,

Wiseman²,

Bolwerk³

et al. 2000

J. Clin. Invest.

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164

146

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Role of Lymphokine in Islet Allograft Rejection

Cited by 34 publications

References 0 publications

Differential Susceptibility of Heart, Skin, and Islet Allografts to T Cell-Mediated Rejection

Differential Susceptibility of Heart, Skin, and Islet Allografts to T Cell-Mediated Rejection

The Degree of Phylogenetic Disparity of Islet Grafts Dictates the Reliance on Indirect CD4 T-Cell Antigen Recognition for Rejection

CD4 T cell–mediated cardiac allograft rejection requires donor but not host MHC class II

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