Evidence map›Paper›PMID 22704961›Full record

ReviewJournal of autoimmunity2012

T cells, murine chronic graft-versus-host disease and autoimmunity.

Robert A Eisenberg, Charles S Via

Abstract readReview
In one paragraph

Review in Journal of autoimmunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

21 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. CD38 Deficiency Ameliorates Chronic Graft-Frontiers in immunology · 2021
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. T-betArthritis research & therapy · 2017
    Article
  16. An update on lupus animal models.Current opinion in rheumatology · 2017
    Review
  17. Article
  18. Article
  19. Article
  20. Autoimmunity in 2012.Clinical reviews in allergy & immunology · 2013
    Review
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 2 institutions in 1 country.

Robert A EisenbergDivision of Rheumatology, Department of Medicine, Perelman School of Medicine at the University of Pennsylvania, 756 BRB II/III, 421 Curie Blvd., Philadelphia, PA 19104-6160, USA. raemd@mail.med.upenn.edu
Charles S Via
Uniformed Services University of the Health Sciences · USUniversity of Pennsylvania · US

Funding

EXPERIMENTAL INDUCTION OF SLE BY ALTERED IAR01AR034156 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI LUNING PRAK, ELINE TJETSKE · 1986 to 2012
$3.5M
Mechanisms of autoreactivity in SLER01AI063626 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI EISENBERG, ROBERT A. · 2005 to 2009
$1.6M
NIAID NIH HHS R01 AI063626NIAMS NIH HHS R01 AR034156
6 · The paper itself

Abstract

The chronic graft-versus-host disease (cGVHD) in mice is characterized by the production of autoantibodies and immunopathology characteristic of systemic lupus erythematosus (lupus). The basic pathogenesis involves the cognate recognition of foreign MHC class II of host B cells by alloreactive CD4 T cells from the donor. CD4 T cells of the host are also necessary for the full maturation of host B cells before the transfer of donor T cells. CD8 T cells play critical roles as well. Donor CD8 T cells that are highly cytotoxic can ablate or prevent the lupus syndrome, in part by killing recipient B cells. Host CD8 T cells can reciprocally downregulate donor CD8 T cells, and thus prevent them from suppressing the autoimmune process. Thus, when the donor inoculum contains both CD4 T cells and CD8 T cells, the resultant syndrome depends on the balance of activities of these various cell populations. For example, in one cGVHD model (DBA/2(C57BL/6xDBA/2)F1, the disease is more severe in females, as it is in several of the spontaneous mouse models of lupus, as well as in human disease. The mechanism of this female skewing of disease appears to depend on the relative inability of CD8 cells of the female host to downregulate the donor CD4 T cells that drive the autoantibody response. In general, then, the abnormal CD4 T cell help and the modulating roles of CD8 T cells seen in cGVHD parallel the participation of T cells in genetic lupus in mice and human lupus, although these spontaneous syndromes are presumably not driven by overt alloreactivity.

Indexed as

AutoimmunityAnimalsAutoantibodiesB-LymphocytesCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCell CommunicationDisease Models, AnimalFemaleGraft vs Host DiseaseHistocompatibility Antigens Class IILupus Erythematosus, SystemicMiceSex FactorsTissue DonorsAutoantibodiesHistocompatibility Antigens Class II

Identifiers

PMID22704961
PMCPMC3578438
OpenAlexW1984511726

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.