Evidence map›Paper›PMID 23136880›Full record

ArticleArthritis research & therapy2012

Modulating proximal cell signaling by targeting Btk ameliorates humoral autoimmunity and end-organ disease in murine lupus.

Jack Hutcheson, Kamala Vanarsa, Anna Bashmakov, Simer Grewal, Deena Sajitharan, Betty Y Chang, Joseph J Buggy, Xin J Zhou, Yong Du, Anne B Satterthwaite and 1 more

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

49 citing papers in PubMed, 94 citations in OpenAlex.

  1. Trial
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  6. Article
  7. Article
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  10. B Cell Aberrance in Lupus: the Ringleader and the Solution.Clinical reviews in allergy & immunology · 2022
    Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Radiosynthesis of [Frontiers in nuclear medicine · 2021
    Article
  17. Emerging B-Cell Therapies in Systemic Lupus Erythematosus.Therapeutics and clinical risk management · 2021
    Review
  18. Article
  19. Review
  20. Review
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

11 authors at 2 institutions in 1 country.

Jack Hutcheson
Kamala Vanarsa
Anna Bashmakov
Simer Grewal
Deena Sajitharan
Betty Y Chang
Joseph J Buggy
Xin J Zhou
Yong Du
Anne B Satterthwaite
Chandra Mohan
The University of Texas Southwestern Medical Center · USPharmacyclics (United States) · US

Funding

LUPUS GENES AND B-CELL SIGNALINGR01AR055600 · NIAMS · UT SOUTHWESTERN MEDICAL CENTER · PI MOHAN, CHANDRA · 2009 to 2013
$1.7M
NIAMS NIH HHS R01 AR055600
6 · The paper itself

Abstract

introductionSystemic lupus erythematosus is a chronic autoimmune disease characterized by an abundance of autoantibodies against nuclear antigens. Bruton's tyrosine kinase (Btk) is a proximal transducer of the BCR signal that allows for B-cell activation and differentiation. Recently, selective inhibition of Btk by PCI-32765 has shown promise in limiting activity of multiple cells types in various models of cancer and autoimmunity. The aim of this study was to determine the effect of Btk inhibition by PCI-32765 on the development of lupus in lupus-prone B6.Sle1 and B6.Sle1.Sle3 mice.

methodsB6.Sle1 or B6.Sle1.Sle3 mice received drinking water containing either the Btk inhibitor PCI-32765 or vehicle for 56 days. Following treatment, mice were examined for clinical and pathological characteristics of lupus. The effect of PCI-32765 on specific cell types was also investigated.

resultsIn this study, we report that Btk inhibition dampens humoral autoimmunity in B6.Sle1 monocongenic mice. Moreover, in B6.Sle1.Sle3 bicongenic mice that are prone to severe lupus, Btk inhibition also dampens humoral and cellular autoimmunity, as well as lupus nephritis.

conclusionsThese findings suggest that partial crippling of cell signaling in B cells and antigen presenting cells (APCs) may be a viable alternative to total depletion of these cells as a therapeutic modality for lupus.

Indexed as

AdenineAgammaglobulinaemia Tyrosine KinaseAnimalsAutoantibodiesAutoimmunityEnzyme-Linked Immunosorbent AssayFemaleFlow CytometryKidneyLupus Erythematosus, SystemicLupus NephritisLymphocytesMaleMice, CongenicMice, Inbred C57BLPiperidinesAdenineAgammaglobulinaemia Tyrosine KinaseAutoantibodiesBtk protein, mouseibrutinibPiperidinesProtein-Tyrosine KinasesPyrazolesPyrimidines

Identifiers

PMID23136880
PMCPMC3674619
OpenAlexW2157486761

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.