Evidence map›Paper›PMID 9379074›Full record

ReviewImmunologic research1997

Gamma delta T-cell help in responses to pathogens and in the development of systemic autoimmunity.

L Wen, A C Hayday

Abstract readReview
PubMed Publisher
In one paragraph

Review in Immunologic research, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. 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.

L WenDepartment of Internal Medicine, Yale University, New Haven, CT 06520, USA.
A C Hayday

Funding

NIAID NIH HHS AI-389932
6 · The paper itself

Abstract

Mice rendered deficient in alpha beta T-cells by single-gene knockout mutation show enhanced levels of autoantibody formation and even some symptoms of autoimmune disease. This is remarkable given that most experimental studies heretofore have indicated that the development of autoimmune disease is highly multigenic, requiring the complementary actions of multiple loci. The basis of the phenomenon in alpha beta T-cell-deficient mice appears to be the provision of help to B-cells by other cells, including gamma delta T-cells. Perhaps surprisingly, gamma delta T-cell help seems quite efficacious, particularly after infection, when it can culminate in the formation of germinal centers. Furthermore, two independent sets of studies reviewed here indicate that significant levels of self-reactive IgG can also be provoked by gamma delta T-cells independent of germinal center formation. The task ahead is to integrate this pathway into the physiologic immune responses to healthy individuals, immunocompromised individuals, and newborns.

Indexed as

AnimalsAutoimmune DiseasesAutoimmunityHumansMiceMice, KnockoutReceptors, Antigen, T-Cell, gamma-deltaT-LymphocytesReceptors, Antigen, T-Cell, gamma-delta

Identifiers

PMID9379074

What OpenQuestion holds

Textmetadata
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.