Evidence map›Paper›PMID 24517431›Full record

ReviewImmunological reviews2014

Innate allorecognition.

Martin H Oberbarnscheidt, Fadi G Lakkis

Abstract readReview
In one paragraph

Review in Immunological reviews, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.3field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 48 citations in OpenAlex.

  1. Hypermutable hotspot enables the rapid evolution of self/non-self recognition genes inProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  2. Review
  3. Donor-recipient mismatch at theScience translational medicine · 2025
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Marine drugs · 2021
    Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Four-Dimensional Imaging of T Cells in Kidney Transplant Rejection.Journal of the American Society of Nephrology : JASN · 2018
    Article
  14. Innate allorecognition by monocytic cells and its role in graft rejection.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2018
    Review
  15. Article
  16. Article
  17. Alarmins and Their Receptors as Modulators and Indicators of Alloimmune Responses.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2017
    Review
  18. Review
  19. What Is Direct Allorecognition?Current transplantation reports · 2016
    Review
  20. A Conversation with Cohn on the Activation of CD4 T Cells.Scandinavian journal of immunology · 2015
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Martin H OberbarnscheidtThomas E. Starzl Transplantation Institute, University of Pittsburgh School of Medicine & University of Pittsburgh Medical Center, Pittsburgh, PA, USA; Department of Surgery, University of Pittsburgh School of Medicine & University of Pittsburgh Medical Center, Pittsburgh, PA, USA.
Fadi G Lakkis
University of Pittsburgh Medical Center · US

Funding

Innate Recognition of Allogeneic Non-SelfR01AI099465 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LAKKIS, FADI G. · 2012 to 2022
$4.1M
NIAID NIH HHS AI099465NIAID NIH HHS R01 AI099465
6 · The paper itself

Abstract

Vertebrates mount strong adaptive immune responses to transplanted organs (allografts), but the mechanisms by which the innate immune system initiates this response are not completely understood. In anti-microbial immunity, non-self molecules associated with pathogens but not present in the host induce the maturation of innate antigen-presenting cells (APCs) by binding to germ-line-encoded receptors. Mature APCs then initiate the adaptive immune response by presenting microbial antigen and providing costimulatory signals to T cells. How allografts activate APCs, however, is less clear, because allografts are presumably sterile. A widely accepted view is that inflammatory or 'danger' molecules released by dying graft cells at the time of transplantation trigger APC maturation and the T-cell response that follows. Alternatively, it has been proposed that the introduction of microbial products during the surgical procedure could also alert the innate immune system to the presence of the transplanted organ. Here, we review why these hypotheses fail to fully explain how the alloimmune response is initiated after transplantation and summarize evidence that recognition of allogeneic non-self by monocytes is a key event in triggering alloimmunity and graft rejection.

Indexed as

Immunity, InnateOrgan TransplantationTransplantation ToleranceAllograftsAnimalsAntigen-Presenting CellsGraft RejectionGraft SurvivalHumansMolecular Sequence DataTreatment Outcomeallorecognitiondendritic cellsinnate immune systemmonocytestransplantation

Identifiers

PMID24517431
PMCPMC3941468
OpenAlexW4233710876

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.