Evidence map›Paper›PMID 7525835›Full record

ArticleThe Journal of experimental medicine1994

CD2 is involved in maintenance and reversal of human alloantigen-specific clonal anergy.

V A Boussiotis, G J Freeman, J D Griffin, G S Gray, J G Gribben, L M Nadler

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
5.2field-weighted citation impact, top 3% 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

28 citing papers in PubMed, 116 citations in OpenAlex.

  1. Review
  2. Review
  3. CD58 Immunobiology at a Glance.Frontiers in immunology · 2021
    Review
  4. CD2 Immunobiology.Frontiers in immunology · 2020
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Identification of a proline-binding motif regulating CD2-triggered T lymphocyte activation.Proceedings of the National Academy of Sciences of the United States of America · 1998
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

6 authors at 1 institution in 1 country.

V A BoussiotisDana-Farber Cancer Institute, Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115.
G J Freeman
J D Griffin
G S Gray
J G Gribben
L M Nadler
Dana-Farber Cancer Institute · US

Funding

THE BIOLOGY AND TREATMENT OF HUMAN LEUKEMIA AND LYMPHOMAP01CA034183 · NCI · DANA-FARBER CANCER INSTITUTE · PI SCHLOSSMAN, STUART F · 1985 to 1994
–
NCI NIH HHS CA-34183NCI NIH HHS CA-40416
6 · The paper itself

Abstract

Induction and maintenance of a state of T cell unresponsiveness to specific alloantigen would have significant implications for human organ transplantation. Using human histocompatibility leukocyte antigen DR7-specific helper T cell clones, we demonstrate that blockade of the B7 family of costimulatory molecules is sufficient to induce alloantigen-specific T cell clonal anergy. Anergized cells do not respond to alloantigen and a variety of costimulatory molecules, including B7-1, B7-2, intercellular adhesion molecule-1 (ICAM-1), and lymphocyte function-associated molecule (LFA)-3. However, after culture in exogenous interleukin (IL)-2 for at least 7 d, anergized cells can respond to alloantigen in the presence of LFA-3. LFA-3 costimulation subsequently restores responsiveness to alloantigen in the presence of previously insufficient costimulatory signals. Expression of CD2R epitope is downregulated on anergic cells and is restored after 7 d of IL-2 culture. The loss of the CD2R is temporally associated with the inability of anergized cells to respond to LFA-3. These results suggest that in addition to blockade of B7 family members, inhibition of CD2 and, potentially, other costimulatory pathways that might reverse anergy will be necessary to maintain prolonged alloantigen-specific tolerance.

Indexed as

Clonal AnergyImmunoconjugatesAbataceptAntigens, CDAntigens, DifferentiationB7-1 AntigenCD2 AntigensCD58 AntigensClone CellsCTLA-4 AntigenEpitopesHLA-DR7 AntigenHumansInterleukin-2IsoantigensMembrane GlycoproteinsAbataceptAntigens, CDAntigens, DifferentiationB7-1 AntigenCD2 AntigensCD58 AntigensCTLA-4 AntigenCTLA4 protein, humanEpitopesHLA-DR7 AntigenImmunoconjugatesInterleukin-2IsoantigensMembrane Glycoproteins

Identifiers

PMID7525835
PMCPMC2191726
OpenAlexW2150368859

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.