Evidence map›Paper›PMID 9207001›Full record

ArticleThe Journal of experimental medicine1997

A role for CD4 in peripheral T cell differentiation.

D R Brown, N H Moskowitz, N Killeen, S L Reiner

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

14 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Impaired survival of T helper cells in the absence of CD4.Proceedings of the National Academy of Sciences of the United States of America · 2001
    Article
  5. Article
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  10. Review
  11. Review
  12. Article
  13. Disruption of the CD4-major histocompatibility complex class II interaction blocks the development of CD4(+) T cells in vivo.Proceedings of the National Academy of Sciences of the United States of America · 1998
    Article
  14. Oral tolerance.Journal of clinical immunology · 1998
    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

4 authors at 2 institutions in 1 country.

D R BrownDepartment of Medicine, Committee on Immunology and Gwen Knapp Center for Lupus and Immunology Research, University of Chicago, Chicago, Illinois 60637, USA.
N H Moskowitz
N Killeen
S L Reiner
University of Chicago · USUniversity of California, San Francisco · US

Funding

INTERDISCIPLINARY TRAINING PROGRAM IN IMMUNOLOGYT32AI007090 · NIAID · UNIVERSITY OF CHICAGO · PI Peter Aidan Savage · 1985 to 2026
$11.7M
Selection of the T Cell Receptor RepertoireR01AI039506 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KILLEEN, NIGEL PATRICK · 1997 to 2006
$1.8M
DEFINING THE BASIS FOR SUSCEPTIBILITY TO LEISHMANIASISK08AI001309 · NIAID · UNIVERSITY OF CHICAGO · PI REINER, STEVEN L · 1994 to 1998
–
CORECEPTOR FUNCTION IN T LYMPHOCYTE DEVELOPMENTR21AI039506 · NIAID · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI KILLEEN, NIGEL P. · 1996 to 1996
–
NIAID NIH HHS AI-01309NIAID NIH HHS AI-07090NIAID NIH HHS AI-39506NIAID NIH HHS R01 AI039506NIAID NIH HHS T32 AI007090
6 · The paper itself

Abstract

Naive CD4+ T helper cells (Th) differentiate into one of two well-defined cell types during immune responses. Mature Th1 and Th2 cells regulate the type of response as a consequence of the unique cytokines that they secrete. CD4 serves a prominent role in potentiating antigen recognition by helper T cells. We have examined the role of CD4 in peripheral T cell differentiation by studying helper T cells from mice with a congenital defect in CD4 expression. After protein immunization or infection with Leishmania major, CD4-deficient mice were incapable of mounting antigen-specific Th2 responses, but retained their Th1 potency. CD4-deficient, T cell receptor transgenic T cells were also incapable of Th2 differentiation after in vitro activation. Expression of a wild-type CD4 transgene corrected the Th2 defect of CD4-deficient mice in all immune responses tested. To investigate the role of the cytoplasmic domain, mice reconstituted with a truncated CD4 molecule were also studied. Expression of the tailless CD4 transgene could not rescue the Th2 defect of CD4-deficient mice immunized with protein or CD4-deficient transgenic T cells activated in vitro, raising the possibility that the cytoplasmic domain of CD4 may influence Th2 generation. Expression of the tailless transgene was, however, capable of restoring Th2 development in CD4-deficient mice infected with L. major or CD4-deficient transgenic T cells activated in the presence of recombinant IL-4, demonstrating that the cytoplasmic domain is not absolutely required for Th2 development. Together, these results demonstrate a previously undescribed role of the CD4 molecule. The requirement for CD4 in Th2 maturation reflects the importance of molecules other than cytokines in the control of helper T cell differentiation.

Indexed as

AnimalsCD4 AntigensCell DifferentiationMiceMice, Inbred BALB CMice, Inbred C57BLMice, TransgenicTh1 CellsTh2 CellsCD4 Antigens

Identifiers

PMID9207001
PMCPMC2198953
OpenAlexW2132256212

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.