Evidence map›Paper›PMID 12699405›Full record

ArticleClinical and experimental immunology2003

Association of stress proteins with autoantigens: a possible mechanism for triggering autoimmunity?

A W Purcell, A Todd, G Kinoshita, T A Lynch, C L Keech, M-J Gething, T P Gordon

Open access · greenAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

24 citing papers in PubMed, 57 citations in OpenAlex.

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  14. Article
  15. Autoantibodies in systemic lupus erythematosus.Pediatric nephrology (Berlin, Germany) · 2012
    Review
  16. Article
  17. Article
  18. Article
  19. An efficient procedure for purification of recombinant human β heat shock protein 90.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2010
    Article
  20. Role of GRP78/BiP degradation and ER stress in deoxynivalenol-induced interleukin-6 upregulation in the macrophage.Toxicological sciences : an official journal of the Society of Toxicology · 2009
    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.

A W PurcellDepartment of Microbiology and Immunology, University of Melbourne, Victoria, Australia. apurcell@unimelb.edu.au
A Todd
G Kinoshita
T A Lynch
C L Keech
M-J Gething
T P Gordon
University of Melbourne · AUFlinders University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Patterns of autoantibody production are diagnostic of many autoimmune disorders; the recent observation of additional autospecificities towards stress-induced proteins may also provide insight into the mechanisms by which such responses arise. Grp78 (also known as BiP) is a target of autoaggressive B and T cell responses in our murine model of anti-Ro (SS-A) autoimmunity and also in rheumatoid arthritis. In this report we demonstrate reciprocal intermolecular spreading occurs between Ro52 and Grp78 in immunized mice, reflecting physiological association of these molecules in vivo. Moreover, we provide direct biochemical evidence that Grp78 associates with the clinically relevant autoantigen, Ro52 (SS-A). Due to the discrete compartmentalization of Ro52 (nucleocytoplasmic) and Grp78 (endoplasmic reticulum; ER) we propose that association of these molecules occurs either in apoptotic cells, where they have been demonstrated indirectly to co-localize in discrete apoptotic bodies, or in B cells themselves where both Ro52 and Grp78 are known to bind to immunoglobulin heavy chains. Tagging of molecules by association with Grp78 may facilitate receptor mediated phagocytotsis of the complex; we show evidence that exogenous Grp78 can associate with cell surface receptors on a subpopulation of murine splenocytes. Given the likelihood that Grp78 will associate with viral glycoproteins in the ER it is possible that it may become a bystander target of the spreading antiviral immune response. Thus, we propose a model whereby immunity elicited towards Grp78 leads to the selection of responses towards the Ro polypeptides and the subsequent cascade of responses observed in human disease.

Indexed as

RNA, Small CytoplasmicAnimalsAutoantibodiesAutoantigensAutoimmunityBinding, CompetitiveCarrier ProteinsEndoplasmic Reticulum Chaperone BiPFluorescent Antibody Technique, IndirectHeat-Shock ProteinsHSP70 Heat-Shock ProteinsHSP90 Heat-Shock ProteinsHumansMiceMice, Inbred C3HMolecular ChaperonesAutoantibodiesAutoantigensCarrier ProteinsEndoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsHSP70 Heat-Shock ProteinsHSP90 Heat-Shock ProteinsHSPA5 protein, humanHspa5 protein, mouseMolecular ChaperonesRibonucleoproteinsRNA, Small CytoplasmicRO60 protein, humanSsa2 protein, mouseSS-A Antigen

Identifiers

PMID12699405
PMCPMC1808692
OpenAlexW2073722224

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.