Evidence map›Paper›PMID 12235211›Full record

ArticleThe Journal of experimental medicine2002

Histidyl-tRNA synthetase and asparaginyl-tRNA synthetase, autoantigens in myositis, activate chemokine receptors on T lymphocytes and immature dendritic cells.

O M Zack Howard, Hui Fang Dong, De Yang, Nina Raben, Kanneboyina Nagaraju, Antony Rosen, Livia Casciola-Rosen, Michael Härtlein, Michael Kron, David Yang and 4 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.

0numbers the graph read from it
0cells of the map it votes in
105citing papers in PubMed
7.0field-weighted citation impact, top 3% 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

105 citing papers in PubMed, 276 citations in OpenAlex.

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  10. A Review of Antisynthetase Syndrome-Associated Interstitial Lung Disease.International journal of molecular sciences · 2024
    Review
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45 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

14 authors at 7 institutions in 3 countries.

O M Zack HowardNational Cancer Institute, Center for Cancer Research, Laboratory of Molecular Immunoregulation, Frederick, MD 21702, USA. howardz@mail.ncifcrf.gov
Hui Fang Dong
De Yang
Nina Raben
Kanneboyina Nagaraju
Antony Rosen
Livia Casciola-Rosen
Michael Härtlein
Michael Kron
David Yang
Kwabena Yiadom
Sunita Dwivedi
Paul H Plotz
Joost J Oppenheim
Georgetown University · USJohns Hopkins University · USNational Institutes of Health · USCancer Institute (WIA) · INInstitut Langevin · FRMichigan State University · USScience Applications International Corporation (United States) · US

Funding

IMMUNOPATHOGEN AUTOIMMUNE INFLAMMATORY MYOPATHIES--POLYMYOSITIS/DERMATOMYOSITISZ01AR041074 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI PLOTZ, PAUL H. · 1988 to 2008
$388k
NCI NIH HHS N01 CO012400NCI NIH HHS N01-CO-12400
6 · The paper itself

Abstract

Autoantibodies to histidyl-tRNA synthetase (HisRS) or to alanyl-, asparaginyl-, glycyl-, isoleucyl-, or threonyl-tRNA synthetase occur in approximately 25% of patients with polymyositis or dermatomyositis. We tested the ability of several aminoacyl-tRNA synthetases to induce leukocyte migration. HisRS induced CD4(+) and CD8(+) lymphocytes, interleukin (IL)-2-activated monocytes, and immature dendritic cells (iDCs) to migrate, but not neutrophils, mature DCs, or unstimulated monocytes. An NH(2)-terminal domain, 1-48 HisRS, was chemotactic for lymphocytes and activated monocytes, whereas a deletion mutant, HisRS-M, was inactive. HisRS selectively activated CC chemokine receptor (CCR)5-transfected HEK-293 cells, inducing migration by interacting with extracellular domain three. Furthermore, monoclonal anti-CCR5 blocked HisRS-induced chemotaxis and conversely, HisRS blocked anti-CCR5 binding. Asparaginyl-tRNA synthetase induced migration of lymphocytes, activated monocytes, iDCs, and CCR3-transfected HEK-293 cells. Seryl-tRNA synthetase induced migration of CCR3-transfected cells but not iDCs. Nonautoantigenic aspartyl-tRNA and lysyl-tRNA synthetases were not chemotactic. Thus, autoantigenic aminoacyl-tRNA synthetases, perhaps liberated from damaged muscle cells, may perpetuate the development of myositis by recruiting mononuclear cells that induce innate and adaptive immune responses. Therefore, the selection of a self-molecule as a target for an autoantibody response may be a consequence of the proinflammatory properties of the molecule itself.

Indexed as

Aspartate-tRNA LigaseRNA, Transfer, Amino AcylAmino Acyl-tRNA SynthetasesAutoantigensCell MovementDendritic CellsHistidine-tRNA LigaseHumansInterleukin-2MyositisReceptors, CCR2Receptors, CCR3Receptors, CCR5Receptors, ChemokineT-LymphocytesVirulence Factors, BordetellaAmino Acyl-tRNA Synthetasesasparaginyl-tRNA synthetaseAspartate-tRNA LigaseAutoantigensCCR2 protein, humanCCR3 protein, humanHistidine-tRNA LigaseInterleukin-2Receptors, CCR2Receptors, CCR3Receptors, CCR5Receptors, ChemokineRNA, Transfer, Amino AcylVirulence Factors, Bordetella

Identifiers

PMID12235211
PMCPMC2194054
OpenAlexW2001220125

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.