Evidence map›Paper›PMID 20958321›Full record

ReviewAnnals of the New York Academy of Sciences2010

A role for calreticulin in the pathogenesis of rheumatoid arthritis.

Joseph Holoshitz, Denise E De Almeida, Song Ling

Open access · greenAbstract readReview
In one paragraph

Review in Annals of the New York Academy of Sciences, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

  1. Identification of Antibodies to Chondrocyte and Synoviocyte Antigens in Equine Osteoarthritis.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2025
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  16. Gender-biased regulation of human IL-17-producing cellsJournal of immune based therapies, vaccines and antimicrobials · 2013
    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

3 authors at 1 institution in 1 country.

Joseph HoloshitzDepartment of Internal Medicine, University of Michigan Medical Center, Ann Arbor, Michigan, USA. jholo@umich.edu
Denise E De Almeida
Song Ling
University of Michigan–Ann Arbor · US

Funding

Vector CoreP30AR048310 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FOX, DAVID ALAN · 2001 to 2010
$5.9M
Immune Modulating HLA-Coded Ligands in Rheumatoid ArthritisR01AR059085 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HOLOSHITZ, JOSEPH · 2011 to 2020
$3.8M
UNIVERSITY OF MICHIGAN MULTIPURPOSE ARTHRITIS CENTERP60AR020557 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI IGNELZI, MICHAEL A · 1986 to 2001
$2.9M
A Class II MHC-Associated Lymphocyte Activation DefectR01AI047331 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HOLOSHITZ, JOSEPH · 2002 to 2006
$1.5M
Class II MHC Allele-Specific Signaling: A New Paradigm in Disease PathogenesisR01GM088560 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HOLOSHITZ, JOSEPH · 2009 to 2012
$1.2M
MHC class II-Associated Endothelial DysfunctionR21AR056786 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HOLOSHITZ, JOSEPH · 2009 to 2010
$379k
Immune dysregulation by the rheumatoid arthritis shared epitopeR21AR055170 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HOLOSHITZ, JOSEPH · 2008 to 2009
$367k
SHARED-USE RESEARCH COMPUTERS10RR002498 · NCRR · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CLARK, VIRGINIA A. · 1985 to 1985
–
NCRR NIH HHS UL1RR02498NIAID NIH HHS AI47331NIAID NIH HHS R01 AI047331NIAMS NIH HHS AR20557NIAMS NIH HHS AR48310NIAMS NIH HHS AR55170NIAMS NIH HHS AR56786NIAMS NIH HHS P30 AR048310NIAMS NIH HHS R01 AR059085NIAMS NIH HHS R21 AR055170NIAMS NIH HHS R21 AR056786NIGMS NIH HHS GM88560NIGMS NIH HHS R01 GM088560
6 · The paper itself

Abstract

Calreticulin (CRT) plays a role in the clearance of dying cells and has been implicated in autoimmunity. Recent evidence indicates that cell surface CRT (csCRT) acts as a signal transducing receptor for the rheumatoid arthritis (RA) shared epitope (SE). The SE binding site on CRT has been mapped to amino acid residues 217-223 in the P-domain. Upon interaction with dendritic cells (DCs), the SE activates potent immune regulatory events. In CD8α(+) DCs, which express higher abundance of csCRT, the SE inhibits the tolerogenic enzyme indoleamine 2,3 dioxygenase with resultant inhibition of regulatory T (Treg) cell differentiation. In CD8α(-) DCs, the SE ligand increases secretion of IL-6 and IL-23 and facilitates generation of Th17 cells, a T cell subset known to play a role in autoimmunity. On the basis of these recent findings, we discuss the possibility that the csCRT may play a pathogenic role in RA by transducing SE-activated Th17-polarizing signals.

Indexed as

AnimalsArthritis, RheumatoidCalreticulinCD8 AntigensCell DifferentiationEpitopesHumansMiceT-Lymphocytes, RegulatoryCalreticulinCD8 AntigensEpitopes

Identifiers

PMID20958321
PMCPMC2959188
OpenAlexW1659935020

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.