Histological criteria for immunological rejection of mouse skin homografts

Wolman, M.; Bleiberg, Ilan; Leibovici, Judith

doi:10.1002/path.1711220102

Cited by 6 publications

(3 citation statements)

References 18 publications

(11 reference statements)

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“…6 D). These data are consistent with the findings of Wolman et al ( 45 ) who reported that skin allograft rejection in BALB/c hosts reflects occlusion of blood vessels at the graft-host border with ischemia of the graft. Unlike islet allografts, skin allografts are highly vulnerable to CD4-mediated rejection ( 1 , 2 ); moreover, A/J donors are fully mismatched from BALB/c at MHC class II alleles (I-A k and I-E k ).…”

Section: Discussionsupporting

confidence: 93%

CD103 Expression Is Required for Destruction of Pancreatic Islet Allografts by CD8+ T Cells

Yang

Wang

Yuan

et al. 2002

The Journal of Experimental Medicine

100

112

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The mechanisms by which CD8 effector populations interact with epithelial layers is a poorly defined aspect of adaptive immunity. Recognition that CD8 effectors have the capacity to express CD103, an integrin directed to the epithelial cell-specific ligand E-cadherin, potentially provides insight into such interactions. To assess the role of CD103 in promoting CD8-mediated destruction of epithelial layers, we herein examined the capacity of mice with targeted disruption of CD103 to reject pancreatic islet allografts. Wild-type hosts uniformly rejected islet allografts, concomitant with the appearance of CD8+CD103+ effectors at the graft site. In contrast, the majority of islet allografts transplanted into CD103−/− hosts survived indefinitely. Transfer of wild-type CD8 cells into CD103−/− hosts elicited prompt rejection of long-surviving islet allografts, whereas CD103−/− CD8 cells were completely ineffectual, demonstrating that the defect resides at the level of the CD8 cell. CD8 cells in CD103−/− hosts exhibited normal effector responses to donor alloantigens in vitro and trafficked normally to the graft site, but strikingly failed to infiltrate the islet allograft itself. These data establish a causal relationship between CD8+CD103+ effectors and destruction of graft epithelial elements and suggest that CD103 critically functions to promote intragraft migration of CD8 effectors into epithelial compartments.

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Section: Discussionsupporting

confidence: 93%

CD103 Expression Is Required for Destruction of Pancreatic Islet Allografts by CD8+ T Cells

Yang

Wang

Yuan

et al. 2002

The Journal of Experimental Medicine

100

112

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“…By contrast, Orai1 KI/KI mice showed significantly prolonged skin allograft survival with a median graft survival of 21.1 days. Five days after transplantation, skin grafted onto wildtype C57BL/6 mice in general showed more pronounced perivascular leukocyte infiltration and occlusion of blood vessels – criteria for rejection of skin allografts (30) – compared to Orai1 KI/KI recipient mice (Fig. 5B).…”

Section: Resultsmentioning

confidence: 98%

Store-Operated Ca2+ Entry through ORAI1 Is Critical for T Cell-Mediated Autoimmunity and Allograft Rejection

McCarl

Khalil

et al. 2010

The Journal of Immunology

134

233

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ORAI1 is the pore-forming subunit of the Ca2+ release-activated Ca2+ (CRAC) channel, which is responsible for store-operated Ca2+ entry in lymphocytes. A role for ORAI1 in T cell function in vivo has been inferred from in vitro studies of T cells from human immunodeficient patients with mutations in ORAI1 and Orai1−/− mice, but a detailed analysis of T cell-mediated immune responses in vivo in mice lacking functional ORAI1 has been missing. We therefore generated Orai1 knock-in mice (Orai1KI/KI) expressing a nonfunctional ORAI1-R93W protein. Homozygosity for the equivalent ORAI1-R91W mutation abolishes CRAC channel function in human T cells resulting in severe immunodeficiency. Homozygous Orai1KI/KI mice die neonatally, but Orai1KI/KI fetal liver chimeric mice are viable and show normal lymphocyte development. T and B cells from Orai1KI/KI mice display severely impaired store-operated Ca2+ entry and CRAC channel function resulting in a strongly reduced expression of several key cytokines including IL-2, IL-4, IL-17, IFN-γ, and TNF-α in CD4+ and CD8+ T cells. Cell-mediated immune responses in vivo that depend on Th1, Th2, and Th17 cell function were severely attenuated in ORAI1-deficient mice. Orai1KI/KI mice lacked detectable contact hypersensitivity responses and tolerated skin allografts significantly longer than wild-type mice. In addition, T cells from Orai1KI/KI mice failed to induce colitis in an adoptive transfer model of inflammatory bowel disease. These findings reaffirm the critical role of ORAI1 for T cell function and provide important insights into the in vivo functions of CRAC channels for T cell-mediated immunity.

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“…The animals used and the transplantation procedures were described in an earlier paper (Wolman, Bleiberg and Leibovici, 1976). The histological techniques were also identical .…”

Section: Methodsmentioning

confidence: 99%

Histological study of homografts showing delayed rejection following levan administration

Leibovici

Wolman

Bleiberg

1978

The Journal of Pathology

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The delaying effect of continued administration of levan on mouse skin homograft rejection was found to be due mainly to inhibition of thrombotic occlusion of the nutrient blood vessels. Levan administration did not appear to affect epidermal regeneration, but it seemed to inhibit degranulation of mast cells, resorption of plasma extravasated during the operation and growth of granulation tissue. The delayed rejection caused by levan treatment was apparently caused by infiltration of the graft by activated mononuclear cells from the blood stream. The phenomenon is believed to represent a late stage of the graft rejection process, its apperance depending on the survival of the graft beyond the stage of vascular occlusion.

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Histological criteria for immunological rejection of mouse skin homografts

Cited by 6 publications

References 18 publications

CD103 Expression Is Required for Destruction of Pancreatic Islet Allografts by CD8+ T Cells

CD103 Expression Is Required for Destruction of Pancreatic Islet Allografts by CD8+ T Cells

Store-Operated Ca2+ Entry through ORAI1 Is Critical for T Cell-Mediated Autoimmunity and Allograft Rejection

Histological study of homografts showing delayed rejection following levan administration

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