BackgroundAtherosclerosis 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.ObjectiveWe here investigate the role of TNIK-deficient B cells in atherosclerosis.ResultsApoE−/−TNIKfl/fl(TNIKBWT) andApoE−/−TNIKfl/flCD19-cre(TNIKBKO) mice received a high cholesterol diet for 10 weeks. Atherosclerotic plaque area did not differ betweenTNIKBKOandTNIKBWTmice, 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 inTNIKBKOmice, 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 inTNIKBKOmice, 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.ConclusionWe here conclude that in hyperlipidemicApoE−/−mice, B cell specific TNIK deficiency does not affect atherosclerosis.