Evidence map›Paper›PMID 16352552›Full record

ArticleJournal of virology2006

Lack of intrinsic CTLA-4 expression has minimal effect on regulation of antiviral T-cell immunity.

Dirk Homann, Wolfgang Dummer, Tom Wolfe, Evelyn Rodrigo, Argyrios N Theofilopoulos, Michael B A Oldstone, Matthias G von Herrath

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

27 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
  2. SLAMF7 (CD319) on activated CD8Cell death and differentiation · 2025
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  20. Immunosuppressive mechanisms during viral infectious diseases.Methods in molecular biology (Clifton, N.J.) · 2011
    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

7 authors at 2 institutions in 1 country.

Dirk HomannBarbara Davis Center for Childhood Diabetes, University of Colorado Health Sciences Center. Mail stop B140, P.O. Box 6511, Aurora, CO 80045, USA. dirk.homann@uchsc.edu
Wolfgang Dummer
Tom Wolfe
Evelyn Rodrigo
Argyrios N Theofilopoulos
Michael B A Oldstone
Matthias G von Herrath
La Jolla Institute for Immunology · USScripps Research Institute · US

Funding

PATHOGENESIS OF PERSISTENT VIRAL INFECTIONR01AI009484 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI OLDSTONE, MICHAEL B · 1985 to 2016
$7.2M
USE OF REGULATORY APCS TO INDUCE/MAINTAIN TOLERANCEU19AI051973 · NIAID · LA JOLLA INST FOR ALLERGY &IMMUNOLGY · PI VON HERRATH, MATTHIAS G. · 2001 to 2005
$4.4M
Viruses and DiabetesR01DK058541 · NIDDK · SCRIPPS RESEARCH INSTITUTE · PI OLDSTONE, MICHAEL B · 2002 to 2005
$1.2M
DNA Vaccination &Regulatory Cells in Type I DiabetesR01DK051091 · NIDDK · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI VON HERRATH, MATTHIAS G. · 2003 to 2006
$1.1M
NEUROBIOLOGIC AND IMMUNOLOGIC ASPECTS OF AGINGT32AG000080 · NIA · SCRIPPS RESEARCH INSTITUTE · PI BUXBAUM, JOEL N · 1985 to 2003
$743k
PATHOGENESIS AND TREATMENT OF AUTOIMMUNE DIABETESR29DK051091 · NIDDK · SCRIPPS RESEARCH INSTITUTE · PI VON HERRATH, MATTHIAS G. · 1996 to 2001
$180k
PATHOGENESIS OF PERSISTENT VIRAL INFECTIONR37AI009484 · NIAID · SCRIPPS RESEARCH INSTITUTE · PI OLDSTONE, MICHAEL B · 1988 to 1997
–
NIAID NIH HHS AI09484NIAID NIH HHS R01 AI009484NIAID NIH HHS U19 AI051973NIAID NIH HHS U19 AI 51973NIA NIH HHS AG-00080NIA NIH HHS T32 AG000080NIDDK NIH HHS DK51091NIDDK NIH HHS DK58541NIDDK NIH HHS R01 DK051091NIDDK NIH HHS R01 DK058541NIDDK NIH HHS R29 DK051091
6 · The paper itself

Abstract

CTLA-4 is considered one of the most potent negative regulators of T-cell activation. To circumvent experimental limitations due to fatal lymphoproliferative disease associated with genetic ablation of CTLA-4, we have used radiation chimeras reconstituted with a mixture of CTLA-4+/+ and CTLA-4-/- bone marrow that retain a normal phenotype and allow the evaluation of long-term T-cell immunity under conditions of intrinsic CTLA-4 deficiency. Following virus infection, we profiled primary, memory, and secondary CD8+ and CD4+ T-cell responses directed against eight different viral epitopes. Our data demonstrate unaltered antigen-driven proliferation, acquisition of effector functions, distribution of epitope hierarchies, T-cell receptor repertoire selection, functional avidities, and long-term memory maintenance in the absence of CTLA-4. Moreover, regulation of memory T-cell survival and homeostatic proliferation, as well as secondary responses, was equivalent in virus-specific CTLA4+/+ and CTL-A-4-/- T-cell populations. Thus, lack of CTLA-4 expression by antigen-specific T cells can be compensated for by extrinsic factors in the presence of CTLA-4 expression by other cells. These findings have implications for the physiologic, pathological, and therapeutic regulation of costimulation.

Indexed as

AnimalsAntigens, CDAntigens, DifferentiationCTLA-4 AntigenGene Expression RegulationGene SilencingLymphocyte ActivationMiceT-Lymphocytes, RegulatoryT-Lymphocyte SubsetsAntigens, CDAntigens, DifferentiationCTLA-4 AntigenCtla4 protein, mouse

Identifiers

PMID16352552
PMCPMC1317527
OpenAlexW2165521534

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.