Evidence map›Paper›PMID 19426232›Full record

ReviewImmunological reviews2009

Molecular mechanisms of T-cell receptor and costimulatory molecule ligation/blockade in autoimmune disease therapy.

Joseph R Podojil, Stephen D Miller

Open access · greenAbstract readReview
In one paragraph

Review in Immunological reviews, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

69 citing papers in PubMed, 137 citations in OpenAlex.

  1. Review
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  15. Topical Diacerein Decreases Skin and Splenic CD11cInternational journal of molecular sciences · 2023
    Article
  16. Review
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9 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Joseph R PodojilDepartment of Microbiology-Immunology and Interdepartmental Immunobiology Center, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
Stephen D Miller
Northwestern University · US

Funding

IMMUNOREGULATION AND PATHOLOGY OF CHRONIC-RELAPSING EAER01NS026543 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MILLER, STEPHEN D · 1988 to 2016
$5.0M
PATHOGENESIS AND IMMUNOREGULATION OF PLP-INDUCED R-EAER01NS030871 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MILLER, STEPHEN D · 1993 to 2010
$3.4M
B7/CD28 MEDIATED COSTIMULATION IN THE PATHOLOGY OF R EAER01NS034819 · NINDS · NORTHWESTERN UNIVERSITY · PI MILLER, STEPHEN D · 1996 to 2003
$1.4M
Mechanisms of CD4+CD25+ T Regulatory Cells in EAER01NS048411 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MILLER, STEPHEN D · 2005 to 2008
$1.3M
NINDS NIH HHS R01 NS026543NINDS NIH HHS R01 NS030871NINDS NIH HHS R01 NS034819NINDS NIH HHS R01 NS048411
6 · The paper itself

Abstract

summaryPro-inflammatory CD4(+) T-cell-mediated autoimmune diseases, such as multiple sclerosis and type 1 diabetes, are hypothesized to be initiated and maintained by activated antigen-presenting cells presenting self antigen to self-reactive interferon-gamma and interleukin-17-producing CD4(+) T-helper (Th) type 1/Th17 cells. To date, the majority of Food and Drug Administration-approved therapies for autoimmune disease primarily focus on the global inhibition of immune inflammatory activity. The goal of ongoing research in this field is to develop both therapies that inhibit/eliminate activated autoreactive cells as well as antigen-specific treatments, which allow for the directed blockade of the deleterious effects of self-reactive immune cell function. According to the two-signal hypothesis, activation of a naive antigen-specific CD4(+) T cell requires both stimulation of the T-cell receptor (TCR) (signal 1) and stimulation of costimulatory molecules (signal 2). There also exists a balance between pro-inflammatory and anti-inflammatory immune cell activity, which is regulated by the type and strength of the activating signal as well as the local cytokine milieu in which the naive CD4(+) T cell is activated. To this end, the majority of ongoing research is focused on the delivery of suboptimal TCR stimulation in the absence of costimulatory molecule stimulation, or potential blockade of stimulatory accessory molecules. Therefore, the signaling pathways involved in the induction of CD4(+) T-cell anergy, as apposed to activation, are topics of intense interest.

Indexed as

AnimalsAntibodies, MonoclonalAntigens, CDAutoimmune DiseasesB7-1 AntigenCD28 AntigensCD4-Positive T-LymphocytesClinical Trials as TopicCTLA-4 AntigenHumansImmunosuppressive AgentsLymphocyte ActivationNFATC Transcription FactorsProtein KinasesReceptors, Antigen, T-CellSignal TransductionAntibodies, MonoclonalAntigens, CDB7-1 AntigenCD28 AntigensCTLA-4 AntigenCTLA4 protein, humanImmunosuppressive AgentsNFATC Transcription FactorsProtein KinasesReceptors, Antigen, T-Cell

Identifiers

PMID19426232
PMCPMC2845642
OpenAlexW1970268927

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.