Evidence map›Paper›PMID 20636809›Full record

ReviewImmunological reviews2010

The power and the promise of restimulation-induced cell death in human immune diseases.

Andrew L Snow, Pushpa Pandiyan, Lixin Zheng, Scott M Krummey, Michael J Lenardo

Abstract readReview
In one paragraph

Review in Immunological reviews, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

56 citing papers in PubMed, 98 citations in OpenAlex.

  1. Article
  2. Article
  3. Immune Aging in Rheumatoid Arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2025
    Review
  4. Review
  5. Lymphopenia in sepsis: a narrative review.Critical care (London, England) · 2024
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. T cell receptor (TCR) signaling in health and disease.Signal transduction and targeted therapy · 2021
    Review
  11. Diacylglycerol Kinase alpha in X Linked Lymphoproliferative Disease Type 1.International journal of molecular sciences · 2021
    Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Observational
  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

5 authors at 1 institution in 1 country.

Andrew L SnowLaboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. snowa@niaid.nih.gov
Pushpa Pandiyan
Lixin Zheng
Scott M Krummey
Michael J Lenardo
National Institute of Allergy and Infectious Diseases · US

Funding

Molecular Mechanisms Of The Autoimmune Lymphoproliferative Syndrome And Other Immunoregulatory DisordersZIAAI000769 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI SU, HELEN · 2009 to 2024
$16.7M
Molecular Mechanisms and Treatment Of Autoimmunity In Man And Animal ModelsZIAAI000717 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI SU, HELEN CHUN-HUI · 2009 to 2025
$13.2M
GENE REGULATORY EVENTS IN ESTABLISHING MATURE T CELL TOLERANCEZIAAI000566 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI SU, HELEN CHUN-HUI · 2009 to 2025
$11.4M
Intramural NIH HHS Z99 AI999999
6 · The paper itself

Abstract

Controlled expansion and contraction of lymphocytes both during and after an adaptive immune response are imperative to sustain a healthy immune system. Both extrinsic and intrinsic pathways of lymphocyte apoptosis are programmed to eliminate cells at the proper time to ensure immune homeostasis. Genetic disorders of apoptosis described in mice and humans have established Fas and Bim as critical pro-apoptotic molecules responsible for T-cell death in response to T-cell receptor restimulation and cytokine withdrawal, respectively. Emerging evidence prompts revision of this classic paradigm, especially for our understanding of restimulation-induced cell death (RICD) and its physiological purpose. Recent work indicates that RICD employs both Fas and Bim for T-cell deletion, dispelling the notion that these molecules are assigned to mutually exclusive apoptotic pathways. Furthermore, new mouse model data combined with our discovery of defective RICD in X-linked lymphoproliferative disease (XLP) patient T cells suggest that RICD is essential for precluding excess T-cell accumulation and associated immunopathology during the course of certain infections. Here, we review how these advances offer a refreshing new perspective on the phenomenon of T-cell apoptosis induced through antigen restimulation, including its relevance to immune homeostasis and potential for therapeutic interventions.

Indexed as

AnimalsApoptosisApoptosis Regulatory ProteinsBcl-2-Like Protein 11fas ReceptorGenetic Diseases, X-LinkedHumansLymphoproliferative DisordersMembrane ProteinsModels, ImmunologicalProto-Oncogene ProteinsReceptors, Antigen, T-CellT-LymphocytesApoptosis Regulatory ProteinsBCL2L11 protein, humanBcl2l11 protein, mouseBcl-2-Like Protein 11fas ReceptorMembrane ProteinsProto-Oncogene ProteinsReceptors, Antigen, T-Cell

Identifiers

PMID20636809
PMCPMC2907538
OpenAlexW2168498914

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.