PuSH - Publikationsserver des Helmholtz Zentrums München: Deficiency of germinal center kinase TRAF2 and NCK-interacting kinase (TNIK) in B cells does not affect atherosclerosis.

Informationen

Hinweise zu Qualitätskriterien von Zeitschriften

Open-Access-Richtlinie der Helmholtz-Gemeinschaft 2016

CC Licencences

Metriken für Publikationen

Navigation

Startseite

English

EVA: Veröffentlichen

Neuer EVA Antrag

Recherche

Erweiterte Suche

Durchblättern nach ...

... HMGU-Autoren/Konsortien

... Organisationsstruktur

... Zeitschriften

... Publikationstypen

... Forschungsdaten

... Arbeitsgruppen

... Erscheinungsjahr

Publikationen im Überblick

Statistik

HGF Fortschrittsbericht

OA Publikationen

Eintragen

Neue Publikation eintragen

Neue Publikation holen aus...

...EVA

Fehlende Publikation melden

Highlights

Suche

Hilfe & Kontakt

Ansprechpartner

Hilfe

Datenschutz

Helmholtz Open Science

Bibliometrische Indikatoren

SHERPA/RoMEO

DOAJ

Export:

Text

Endnote (RIS) BIB

BibTeX

van Os, B.W.* ; Kusters, P.J.H.* ; den Toom, M.* ; Beckers, L.* ; van Tiel, C.M.* ; Vos, W.G.* ; de Jong, E.* ; Kieser, A. ; van Roomen, C.* ; Binder, C.J.* ; Reiche, M.E.* ; de Winther, M.P.* ; Bosmans, L.A.* ; Lutgens, E.*

Deficiency of germinal center kinase TRAF2 and NCK-interacting kinase (TNIK) in B cells does not affect atherosclerosis.

Front. Cardiovasc. Med. 10:1171764 (2023)

Verlagsversion

DOI

PMC

	Open Access Gold

Abstract
Metriken
Zusatzinfos

BACKGROUND: Atherosclerosis is the underlying cause of many cardiovascular diseases, such as myocardial infarction or stroke. B cells, and their production of pro- and anti-atherogenic antibodies, play an important role in atherosclerosis. In B cells, TRAF2 and NCK-interacting Kinase (TNIK), a germinal center kinase, was shown to bind to TNF-receptor associated factor 6 (TRAF6), and to be involved in JNK and NF-κB signaling in human B cells, a pathway associated with antibody production. OBJECTIVE: We here investigate the role of TNIK-deficient B cells in atherosclerosis. RESULTS: ApoE^-/-TNIK^fl/fl (TNIK^BWT) and ApoE^-/-TNIK^fl/flCD19-cre (TNIK^BKO) mice received a high cholesterol diet for 10 weeks. Atherosclerotic plaque area did not differ between TNIK^BKO and TNIK^BWT mice, nor was there any difference in plaque necrotic core, macrophage, T cell, α-SMA and collagen content. B1 and B2 cell numbers did not change in TNIK^BKO mice, and marginal zone, follicular or germinal center B cells were unaffected. Total IgM and IgG levels, as well as oxidation specific epitope (OSE) IgM and IgG levels, did not change in absence of B cell TNIK. In contrast, plasma IgA levels were decreased in TNIK^BKO mice, whereas the number of IgA⁺ B cells in intestinal Peyer's patches increased. No effects could be detected on T cell or myeloid cell numbers or subsets. CONCLUSION: We here conclude that in hyperlipidemic ApoE^-/- mice, B cell specific TNIK deficiency does not affect atherosclerosis.

Impact Factor

Scopus SNIP

Altmetric

3.600

0.000