Evidence map›Paper›PMID 22993205›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

Thymic function is maintained during Salmonella-induced atrophy and recovery.

Ewan A Ross, Ruth E Coughlan, Adriana Flores-Langarica, Sian Lax, Julia Nicholson, Guillaume E Desanti, Jennifer L Marshall, Saeeda Bobat, Jessica Hitchcock, Andrea White and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. 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
1.9field-weighted citation impact, top 14% 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, 43 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. T cell regeneration after immunological injury.Nature reviews. Immunology · 2021
    Review
  8. Infection-Associated Thymic Atrophy.Frontiers in immunology · 2021
    Review
  9. Control of PersistentPathogens (Basel, Switzerland) · 2020
    Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
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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

17 authors at 3 institutions in 1 country.

Ewan A RossMedical Research Council Centre for Immune Regulation, School of Immunity and Infection, Institute for Biomedical Research, Medical School, University of Birmingham, Edgbaston, Birmingham, B15 2TT, United Kingdom.
Ruth E Coughlan
Adriana Flores-Langarica
Sian Lax
Julia Nicholson
Guillaume E Desanti
Jennifer L Marshall
Saeeda Bobat
Jessica Hitchcock
Andrea White
William E Jenkinson
Mahmood Khan
Ian R Henderson
Gareth G Lavery
Christopher D Buckley
Graham Anderson
Adam F Cunningham
Medical Research Council · GBUniversity of Birmingham · GBImmune Regulation (United Kingdom) · GB

Funding

Biotechnology and Biological Sciences Research Council BB/F022778/1Biotechnology and Biological Sciences Research Council BB/G023468/1Medical Research Council G0401620Medical Research Council G0900857Medical Research Council G1001055Medical Research Council G1001390Wellcome Trust 090244
6 · The paper itself

Abstract

Thymic atrophy is a frequent consequence of infection with bacteria, viruses, and parasites and is considered a common virulence trait between pathogens. Multiple reasons have been proposed to explain this atrophy, including premature egress of immature thymocytes, increased apoptosis, or thymic shutdown to prevent tolerance to the pathogen from developing. The severe loss in thymic cell number can reflect an equally dramatic reduction in thymic output, potentially reducing peripheral T cell numbers. In this study, we examine the relationship between systemic Salmonella infection and thymic function. During infection, naive T cell numbers in peripheral lymphoid organs increase. Nevertheless, this occurs despite a pronounced thymic atrophy caused by viable bacteria, with a peak 50-fold reduction in thymocyte numbers. Thymic atrophy is not dependent upon homeostatic feedback from peripheral T cells or on regulation of endogenous glucocorticoids, as demonstrated by infection of genetically altered mice. Once bacterial numbers fall, thymocyte numbers recover, and this is associated with increases in the proportion and proliferation of early thymic progenitors. During atrophy, thymic T cell maturation is maintained, and single-joint TCR rearrangement excision circle analysis reveals there is only a modest fall in recent CD4(+) thymic emigrants in secondary lymphoid tissues. Thus, thymic atrophy does not necessarily result in a matching dysfunctional T cell output, and thymic homeostasis can constantly adjust to systemic infection to ensure that naive T cell output is maintained.

Indexed as

AnimalsAtrophyCD4-Positive T-LymphocytesCell DifferentiationCell MovementMiceRecovery of FunctionSalmonella InfectionsSalmonella typhimuriumThymus Gland

Identifiers

PMID22993205
PMCPMC3912538
OpenAlexW2133157954

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.