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.
Highlights
The v-abl Abelson murine leukemia viral oncogene 2 (Abl2), or Abelson related gene (Arg), encodes a non-receptor tyrosine Abl kinase, which together with c-Abl (Abl1) comprises the family of Abl tyrosine kinases [1]
In a recent article [14], we described the role for Arg in development of Myelin Oligodendrocyte Glycoprotein (MOG35-55)induced, T-cell dependent experimental autoimmune encephalomyelitis (EAE), a widely used experimental model for multiple sclerosis (MS)
One could argue that if the disease development we observe as a result of MOG(35-55) immunization in the Arg-/- mice is due to c-Abl rescuing a T-cell response, induction of EAE with whole MOG protein might be more interactive with signaling pathways involving Arg
Summary
The v-abl Abelson murine leukemia viral oncogene 2 (Abl2), or Abelson related gene (Arg), encodes a non-receptor tyrosine Abl kinase, which together with c-Abl (Abl1) comprises the family of Abl tyrosine kinases [1]. These studies show an important role for the Abl/Arg kinases in T-cell activation.
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