Evidence map›Paper›PMID 21841129›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2011

B cells and TCR avidity determine distinct functions of CD4+ T cells in retroviral infection.

Mickaël J-Y Ploquin, Urszula Eksmond, George Kassiotis

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.5field-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

30 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. CD4Nature immunology · 2023
    Review
  5. Individual Epitope-Specific CD8Pathogens (Basel, Switzerland) · 2023
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. CD4Cell reports · 2020
    Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

3 authors at 2 institutions in 1 country.

Mickaël J-Y PloquinDivision of Immunoregulation, Medical Research Council National Institute for Medical Research, The Ridgeway, London NW7 1AA, United Kingdom.
Urszula Eksmond
George Kassiotis
General Medical Council · GBMedical Research Council · GB

Funding

Medical Research Council MC_U117581330Medical Research Council U.1175.02.006.00007(81330)Medical Research Council U117581330
6 · The paper itself

Abstract

The T cell-dependent B cell response relies on cognate interaction between B cells and CD4(+) Th cells. However, the consequences of this interaction for CD4(+) T cells are not entirely known. B cells generally promote CD4(+) T cell responses to pathogens, albeit to a variable degree. In contrast, CD4(+) T cell responses to self- or tumor Ags are often suppressed by B cells. In this study, we demonstrated that interaction with B cells dramatically inhibited the function of virus-specific CD4(+) T cells in retroviral infection. We have used Friend virus infection of mice as a model for retroviral infection, in which the behavior of virus-specific CD4(+) T cells was monitored according to their TCR avidity. We report that avidity for Ag and interaction with B cells determine distinct aspects of the primary CD4(+) T cell response to Friend virus infection. Virus-specific CD4(+) T cells followed exclusive Th1 and T follicular helper (Tfh) differentiation. High avidity for Ag facilitated expansion during priming and enhanced the capacity for IFN-γ and IL-21 production. In contrast, Tfh differentiation was not affected by avidity for Ag. By reducing or preventing B cell interaction, we found that B cells promoted Tfh differentiation, induced programmed death 1 expression, and inhibited IFN-γ production by virus-specific CD4(+) T cells. Ultimately, B cells protected hosts from CD4(+) T cell-mediated immune pathology, at the detriment of CD4(+) T cell-mediated protective immunity. Our results suggest that B cell presentation of vaccine Ags could be manipulated to direct the appropriate CD4(+) T cell response.

Indexed as

Adoptive TransferAnimalsAntigen PresentationB-LymphocytesCD4-Positive T-LymphocytesCell DifferentiationCell SeparationFlow CytometryFriend murine leukemia virusGene Expression ProfilingLymphocyte ActivationMiceMice, Inbred C57BLMice, TransgenicProtein BindingReceptors, Antigen, T-CellReceptors, Antigen, T-Cell

Identifiers

PMID21841129
PMCPMC3173872
OpenAlexW2134173374

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.