Evidence map›Paper›PMID 24203440›Full record

ReviewImmunologic research2013

Autoimmune effector memory T cells: the bad and the good.

Priyadharshini Devarajan, Zhibin Chen

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Immunologic research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05345197 (Emicizumab in Patients With Acquired Hemophilia A), which is not on this map. Cited by 57 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 2 pooled it
2.9field-weighted citation impact, top 9% 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.

NCT05345197 phase2active not recruitingnot on this mapstarted 2022, after this paper: background citation

Emicizumab in Patients With Acquired Hemophilia A: Multicenter, Single-arm, Open-label Clinical Trial

TypeinterventionalSponsorUniversity of WashingtonRan2022 to 2026Enrolled51ConditionsAcquired Hemophilia AArmsemicizumab
3 · Its place in the literature

Who cites it

57 citing papers in PubMed, 2 syntheses or guidelines pooled it, 105 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. IL-15/NKG2D signaling-mediated activation of CD8Journal of thoracic disease · 2026
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  17. Frontiers in immunology · 2023
    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

2 authors at 1 institution in 1 country.

Priyadharshini DevarajanDepartment of Microbiology and Immunology, University of Miami Miller School of Medicine, RMSB 3035, 1600 NW 10th Ave, Miami, FL, 33136, USA.
Zhibin Chen
University of Miami · US

Funding

The quantitative biology of CTLA4 splice variants in T1DDP3DK085696 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI CHEN, ZHIBIN · 2009 to 2009
$2.3M
NIDDK NIH HHS DP3 DK085696NIDDK NIH HHS #DP3DK085696
6 · The paper itself

Abstract

Immunological memory is a hallmark of adaptive immunity, a defense mechanism endowed to vertebrates during evolution. However, an autoimmune pathogenic role of memory lymphocytes is also emerging with accumulating evidence, despite reasonable skepticism on their existence in a chronic setting of autoimmune damage. It is conceivable that autoimmune memory would be particularly harmful since memory cells would constantly "remember" and attack the body's healthy tissues. It is even more detrimental given the resistance of memory T cells to immunomodulatory therapies. In this review, we focus on self-antigen-reactive CD(+) effector memory T (TEM) cells, surveying the evidence for the role of the T(EM) compartment in autoimmune pathogenesis. We will also discuss the role of T(EM) cells in chronic and acute infectious disease settings and how they compare to their counterparts in autoimmune diseases. With their long-lasting potency, the autoimmune T(EM) cells could also play a critical role in anti-tumor immunity, which may be largely based on their reactivity to self-antigens. Therefore, although autoimmune T(EM) cells are "bad" due to their role in relentless perpetration of tissue damage in autoimmune disease settings, they are unlikely a by-product of industrial development along the modern surge of autoimmune disease prevalence. Rather, they may be a product of evolution for their "good" in clearing damaged host cells in chronic infections and malignant cells in cancer settings.

Indexed as

AnimalsAutoimmune DiseasesAutoimmunityCTLA-4 AntigenHumansImmunologic MemoryNeoplasmsT-Lymphocyte SubsetsCTLA-4 Antigen

Identifiers

PMID24203440
PMCPMC4067599
OpenAlexW1970350730

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.