Evidence map›Paper›PMID 31597758›Full record

ArticleJournal of virology2019

B Cell-Intrinsic SHP1 Expression Promotes the Gammaherpesvirus-Driven Germinal Center Response and the Establishment of Chronic Infection.

K E Johnson, P T Lange, C N Jondle, P J Volberding, U M Lorenz, W Cui, B N Dittel, V L Tarakanova

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-weighted citation impact, top 26% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
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  5. Gammaherpesvirus-mediated repression reveals EWSR1 to be a negative regulator of B cell responses.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  6. Article
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  8. Review
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  10. 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

8 authors at 3 institutions in 1 country.

K E JohnsonDepartment of Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
P T LangeDepartment of Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
C N JondleDepartment of Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
P J VolberdingDepartment of Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
U M LorenzDepartment of Microbiology, Immunology, and Cancer Biology, University of Virginia School of Medicine, Charlottesville, Virginia, USA.
W CuiDepartment of Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
B N DittelDepartment of Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
V L TarakanovaDepartment of Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA vtarakan@mcw.edu.
Medical College of Wisconsin · USVersiti Blood Center of Wisconsin · USCarter Center · US

Funding

The Cellular and Transcriptional Control of CD8 T Cell Functional Adaptation to Chronic VirusesR01AI125741 · NIAID · VERSITI WISCONSIN, INC. · PI CUI, WEIGUO · 2016 to 2020
$2.1M
IRF-1: a brake to limit gammaherpesvirus infection and pathogenesisR01CA203923 · NCI · MEDICAL COLLEGE OF WISCONSIN · PI TARAKANOVA, VERA L. · 2017 to 2021
$2.0M
ATM and gammaherpesvirus infection: a precarious balanceR01CA183593 · NCI · MEDICAL COLLEGE OF WISCONSIN · PI TARAKANOVA, VERA L. · 2014 to 2018
$1.6M
B cell-mediated immune regulationR56AI129348 · NIAID · VERSITI WISCONSIN, INC. · PI DITTEL, BONNIE N · 2017 to 2017
$451k
Not just acute: IRF-7 has two site-specific functions against chronic gammaherpesvirus infectionF31CA243364 · NCI · MEDICAL COLLEGE OF WISCONSIN · PI JOHNSON, KAITLIN E · 2019 to 2020
$45k
NCI NIH HHS F31 CA243364NCI NIH HHS R01 CA183593NCI NIH HHS R01 CA203923NIAID NIH HHS R01 AI125741NIAID NIH HHS R56 AI129348
6 · The paper itself

Abstract

Gammaherpesviruses are ubiquitous pathogens that establish lifelong infections in the majority of adults worldwide. Chronic gammaherpesvirus infection has been implicated in both lymphomagenesis and, somewhat controversially, autoimmune disease development. Pathogenesis is largely associated with the unique ability of gammaherpesviruses to usurp B cell differentiation, specifically, the germinal center response, to establish long-term latency in memory B cells. The host tyrosine phosphatase SHP1 is known as a brake on immune cell activation and is downregulated in several gammaherpesvirus-driven malignancies. However, here we demonstrate that B cell- but not T cell-intrinsic SHP1 expression supports the gammaherpesvirus-driven germinal center response and the establishment of viral latency. Furthermore, B cell-intrinsic SHP1 deficiency cooperated with gammaherpesvirus infection to increase the levels of double-stranded DNA-reactive antibodies at the peak of viral latency. Thus, in spite of decreased SHP1 levels in gammaherpesvirus-driven B cell lymphomas, B cell-intrinsic SHP1 expression plays a proviral role during the establishment of chronic infection, suggesting that the gammaherpesvirus-SHP1 interaction is more nuanced and is modified by the stage of infection and pathogenesis.

Indexed as

AnimalsAntibodies, AntinuclearB-LymphocytesChronic DiseaseDNAFemaleGerminal CenterHerpesviridae InfectionsHost-Pathogen InteractionsHumansImmunologic MemoryLymphocyte ActivationMaleMiceMice, TransgenicPrimary Cell CultureAntibodies, AntinuclearDNAProtein Tyrosine Phosphatase, Non-Receptor Type 6gammaherpesvirusgerminal center B cellSHP1

Identifiers

PMID31597758
PMCPMC6912115
OpenAlexW2978480551

What OpenQuestion holds

Textmetadata
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.