ArticleThe Journal of experimental medicine2002
CD103 expression is required for destruction of pancreatic islet allografts by CD8(+) T cells.
Article in The Journal of experimental medicine, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
37 citing papers in PubMed.
- Origins of CD8 tissue resident memory.Frontiers in immunology · 2026Review
- Evolving role of CD8Frontiers in immunology · 2026Review
- Genetic predisposition to early mycosis fungoides: investigating genetic polymorphisms in tissue-resident memory T-cell genes.The Journal of international medical research · 2024Article
- Renal graft function in transplanted patients correlates with CD45RC T cell phenotypic signature.PloS one · 2024Article
- Immunotherapy and Liver Transplantation: A Narrative Review of Basic and Clinical Data.Cancers · 2023Review
- CD103Immune network · 2023Article
- Single-Cell Landscape of Mouse Islet Allograft and Syngeneic Graft.Frontiers in immunology · 2022Article
- The molecular basis and cellular effects of distinct CD103 expression on CD4 and CD8 T cells.Cellular and molecular life sciences : CMLS · 2021Article
- Resident memory T cells form during persistent antigen exposure leading to allograft rejection.Science immunology · 2021Article
- Programmed T cell differentiation: Implications for transplantation.Cellular immunology · 2020Review
- An anti-CD103 antibody-drug conjugate prolongs the survival of pancreatic islet allografts in mice.Cell death & disease · 2019Article
- Immunohistopathological characterization and the impact of topical immunomodulatory therapy in oral chronic graft-versus-host disease: A pilot study.Oral diseases · 2018Article
- Transcriptional programming of tissue-resident memory CD8Current opinion in immunology · 2018Review
- Resident Memory-Like Tumor-Infiltrating Lymphocytes (TILFrontiers in immunology · 2018Review
- The Emerging Role of CD8Frontiers in immunology · 2018Review
- Environmental cues orchestrate regional immune surveillance and protection by pulmonary CTLs.Journal of leukocyte biology · 2016Review
- CD103+ Dendritic Cells Elicit CD8+ T Cell Responses to Accelerate Kidney Injury in Adriamycin Nephropathy.Journal of the American Society of Nephrology : JASN · 2016Article
- Bone Marrow T Cells and the Integrated Functions of Recirculating and Tissue-Resident Memory T Cells.Frontiers in immunology · 2016Review
- The emerging role of resident memory T cells in protective immunity and inflammatory disease.Nature medicine · 2015Review
- Smad4 promotes differentiation of effector and circulating memory CD8 T cells but is dispensable for tissue-resident memory CD8 T cells.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
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6 authors.
Funding
Abstract
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.