B-cells and Inflammation in the Absence of the Abelson Related Gene (Arg)

Abstract

The Abelson non-receptor tyrosine kinases, c-Abl and Arg, are important regulators of cellular processes in cancer, inflammation, infection, and neuronal dynamics. Recent research on the role for these kinases in processes involving interactions with the cytoskeleton or signaling molecules, may lead to further insight into the pathogenesis of a variety of disorders, including chronic inflammatory diseases. In a mouse model for multiple sclerosis, we recently reported that Arg deficient mice develop T-cell mediated autoimmune neuro-inflammation with the same severity as littermate controls, but display a different B-cell phenotype upon immunization. Here we comment on these results and discuss the role for Arg in B-cell activation and homeostasis.

A Role for the Non-Receptor Tyrosine Kinase Abl2/Arg in Experimental Neuroinflammation

“…Considering that c-Abl and Arg share more than 90% structure and domain similarities in their N-terminal parts (Koleske et al, 1998 ), comprising the SH2, SH3 and kinase domains (Fig. 7 ), and that the protein level of Arg is high in mature B cells compared to c-Abl (Bianchi et al, 2002 ), Arg could similarly be an important actor in B-cell activation and proliferation (Andersson and Aksel Jacobsen, 2016 ). Herein presented data reveal an altered B- and T-cell phenotype in MBP 89–101 immunized congenic mice, homozygous for Eae27 inherited from the RIIIS/J donor strain, when stimulated in vitro.…”