Evidence map›Paper›PMID 20675588›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2010

Neutrophil functions and autoimmune arthritis in the absence of p190RhoGAP: generation and analysis of a novel null mutation in mice.

Tamás Németh, Krisztina Futosi, Csilla Hably, Madeleine R Brouns, Sascha M Jakob, Miklós Kovács, Zsuzsanna Kertész, Barbara Walzog, Jeffrey Settleman, Attila Mócsai

Open access · greenAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 41 citations in OpenAlex.

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  12. Glucocorticoid receptor DNA binding factor 1 expression and osteosarcoma prognosis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
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  15. Endobiogeny: a global approach to systems biology (part 2 of 2).Global advances in health and medicine · 2013
    Review
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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

10 authors at 5 institutions in 5 countries.

Tamás NémethDepartment of Physiology, Semmelweis University School of Medicine, Budapest, Hungary.
Krisztina Futosi
Csilla Hably
Madeleine R Brouns
Sascha M Jakob
Miklós Kovács
Zsuzsanna Kertész
Barbara Walzog
Jeffrey Settleman
Attila Mócsai
Semmelweis University · HUCzech Academy of Sciences, Institute of Physiology · CZMassachusetts General Hospital · USCentre of Experimental Medicine of the Slovak Academy of Sciences · SKLudwig-Maximilians-Universität München · DE

Funding

European Research Council 206283Wellcome Trust 087782
6 · The paper itself

Abstract

Beta(2) integrins of neutrophils play a critical role in innate immune defense, but they also participate in tissue destruction during autoimmune inflammation. p190RhoGAP (ArhGAP35), a regulator of Rho family small GTPases, is required for integrin signal transduction in fibroblasts. Prior studies have also suggested a role for p190RhoGAP in beta(2) integrin signaling in neutrophils. To directly test that possibility, we have generated a novel targeted mutation completely disrupting the p190RhoGAP-encoding gene in mice. p190RhoGAP deficiency led to perinatal lethality and defective neural development, precluding the analysis of neutrophil functions in adult p190RhoGAP(-/-) animals. This was overcome by transplantation of fetal liver cells from p190RhoGAP(-/-) fetuses into lethally irradiated wild-type recipients. Neutrophils from such p190RhoGAP(-/-) bone marrow chimeras developed normally and expressed normal levels of various cell surface receptors. Although p190RhoGAP(-/-) neutrophils showed moderate reduction of beta(2) integrin-mediated adherent activation, they showed mostly normal migration in beta(2) integrin-dependent in vitro and in vivo assays and normal beta(2) integrin-mediated killing of serum-opsonized Staphylococcus aureus and Escherichia coli. A neutrophil- and beta(2) integrin-dependent transgenic model of the effector phase of autoimmune arthritis also proceeded normally in p190RhoGAP(-/-) bone marrow chimeras. In contrast, all the above responses were completely blocked in CD18(-/-) neutrophils or CD18(-/-) bone marrow chimeras. These results suggest that p190RhoGAP likely does not play a major indispensable role in beta(2) integrin-mediated in vitro and in vivo neutrophil functions or the effector phase of experimental autoimmune arthritis.

Indexed as

AnimalsArthritis, ExperimentalAutoimmune DiseasesBone Marrow CellsCD18 AntigensCells, CulturedClone CellsDisease Models, AnimalGTPase-Activating ProteinsGuanine Nucleotide Exchange FactorsHumansMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMutationARHGAP35 protein, humanArhgap35 protein, mouseCD18 AntigensGTPase-Activating ProteinsGuanine Nucleotide Exchange FactorsRepressor Proteins

Identifiers

PMID20675588
PMCPMC3064944
OpenAlexW2101739026

What OpenQuestion holds

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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.