Evidence map›Paper›PMID 23794629›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2013

Macrophage scavenger receptor 1 (Msr1, SR-A) influences B cell autoimmunity by regulating soluble autoantigen concentration.

Stefanie Haasken, Jennifer L Auger, Justin J Taylor, Patricia M Hobday, Brian D Goudy, Philip J Titcombe, Daniel L Mueller, Bryce A Binstadt

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.4field-weighted citation impact, top 33% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Macrophage regulation of graft-World journal of clinical cases · 2020
    Review
  8. 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

8 authors at 2 institutions in 1 country.

Stefanie HaaskenDepartment of Pediatrics, Center for Immunology, University of Minnesota, Minneapolis, MN 55414, USA.
Jennifer L Auger
Justin J Taylor
Patricia M Hobday
Brian D Goudy
Philip J Titcombe
Daniel L Mueller
Bryce A Binstadt
University of Minnesota Medical Center · USUniversity of Minnesota · US

Funding

TRAINING GRANT IN MICROBIOLOGY/CANCER RESEARCHT32CA009138 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI Scott M. Dehm · 1985 to 2026
$11.3M
IMMUNOLOGY TRAINING PROGRAMT32AI007313 · NIAID · UNIVERSITY OF MINNESOTA TWIN CITIES · PI Carla Rothlin · 1989 to 2026
$5.7M
Characterization of a New Mouse Model of Autoimmune Cardiac Valve DiseaseK08AR054317 · NIAMS · UNIVERSITY OF MINNESOTA · PI BINSTADT, BRYCE · 2007 to 2011
$644k
NCI NIH HHS T32 CA009138NIAID NIH HHS T32 AI007313NIAID NIH HHS T32-AI007313NIAMS NIH HHS K08 AR054317NIAMS NIH HHS K08-AR054317
6 · The paper itself

Abstract

The class A macrophage scavenger receptor Msr1 (SR-A, CD204) has been reported to participate in the maintenance of immunological tolerance. We investigated the role of Msr1 in a mouse model of autoantibody-dependent arthritis. Genetic deficiency of Msr1 in K/BxN TCR transgenic mice decreased the incidence and severity of arthritis because of decreased autoantibody production. Despite normal initial activation of autoreactive CD4(+) T cells, potentially autoreactive B cells in Msr1(-/-) K/BxN mice retained a naive phenotype and did not expand. This was not due to an intrinsic B cell defect. Rather, we found that macrophages lacking Msr1 were inefficient at taking up the key autoantigen glucose-6-phosphate isomerase and that Msr1-deficient mice had elevated serum concentrations of glucose-6-phosphate isomerase. Arthritis developed normally when bone marrow from Msr1(-/-) K/BxN mice was transplanted into hosts whose macrophages did express Msr1. Thus, Msr1 can regulate the concentration of a soluble autoantigen. In this model, the absence of Msr1 led to higher levels of soluble autoantigen and protected mice from developing pathogenic autoantibodies, likely because of altered cognate interactions of autoreactive T and B cells with impaired differentiation of follicular Th cells.

Indexed as

AutoimmunityAnimalsArthritis, ExperimentalAutoantibodiesAutoantigensB-LymphocytesCD4-Positive T-LymphocytesGlucose-6-Phosphate IsomeraseLymphocyte ActivationMacrophagesMiceMice, Inbred C57BLMice, KnockoutScavenger Receptors, Class AAutoantibodiesAutoantigensGlucose-6-Phosphate IsomeraseMsr1 protein, mouseScavenger Receptors, Class A

Identifiers

PMID23794629
PMCPMC3720797
OpenAlexW2146669161

What OpenQuestion holds

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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.