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B-cells and Inflammation in the Absence of the Abelson Related Gene (Arg)
Halmstad University, School of Business, Engineering and Science, The Rydberg Laboratory for Applied Sciences (RLAS). University of Copenhagen, Copenhagen, Denmark.
Copenhagen University, Copenhagen, Denmark.
2016 (English)In: Journal of Clinical & Cellular Immunology, ISSN 2155-9899, E-ISSN 2155-9899, Vol. 7, no 6, 1000470Article in journal (Refereed) Published
Abstract [en]

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.

Place, publisher, year, edition, pages
Los Angeles, CA: Omics Publishing Group , 2016. Vol. 7, no 6, 1000470
Keyword [en]
Arg/Abl2, c-Abl, Experimental autoimmune encephalomyelitis (EAE), B-cells
National Category
Immunology in the medical area
URN: urn:nbn:se:hh:diva-32443DOI: 10.4172/2155-9899.1000470OAI: diva2:1047629
Available from: 2016-11-18 Created: 2016-11-18 Last updated: 2016-11-28Bibliographically approved

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