Arg Deficiency Does not Influence the Course of Myelin Oligodendrocyte Glycoprotein (MOG35-55)-induced Experimental Autoimmune Encephalomyelitis
2016 (English)In: Journal of Clinical & Cellular Immunology, ISSN 2155-9899, E-ISSN 2155-9899, Vol. 7, no 3, 1000420Article in journal (Refereed) Published
Background: Inhibition of Abl kinases has an ameliorating effect on the rodent model for multiple sclerosis, experimental autoimmune encephalomyelitis, and arrests lymphocyte activation. The family of Abl kinases consists of the Abl1/Abl and Abl2/Arg tyrosine kinases. While the Abl kinase has been extensively studied in immune activation, roles for Arg are incompletely characterized. To investigate the role for Arg in experimental autoimmune encephalomyelitis, we studied disease development in Arg-/- mice.
Methods: Arg-/- and Arg+/+ mice were generated from breeding of Arg+/- mice on the C57BL/6 background. Mice were immunized with the myelin oligodendrocyte glycoprotein (MOG)35-55 peptide and disease development recorded. Lymphocyte phenotypes of wild type Arg+/+ and Arg-/- mice were studied by in vitro stimulation assays and flow cytometry.
Results: The breeding of Arg+/+ and Arg-/- mice showed skewing in the frequency of born Arg-/- mice. Loss of Arg function did not affect development of experimental autoimmune encephalomyelitis, but reduced the number of splenic B-cells in Arg-/- mice following immunization with MOG peptide.
Conclusions: Development of MOG-induced experimental autoimmune encephalomyelitis is not dependent on Arg, but Arg plays a role for the number of B cells in immunized mice. This might suggest a novel role for the Arg kinase in B-cell trafficking or regulation. Furthermore, the results suggest that Arg is important for normal embryonic development. © 2016 Jacobsen FA, et al.
Place, publisher, year, edition, pages
Los Angeles: OMICS , 2016. Vol. 7, no 3, 1000420
Abelson related gene, Experimental autoimmune encephalomyelitis, Lymphocyte phenotypes, Genotype frequency
Immunology in the medical area
IdentifiersURN: urn:nbn:se:hh:diva-33668DOI: 10.4172/2155-9899.1000420OAI: oai:DiVA.org:hh-33668DiVA: diva2:1086903
Funding: Novo Nordisk, Denmark; SHARE (Synergy in human and animal research) Copenhagen University; The Warwara Larsen Foundation, The Carlsberg Foundation; The Karen A Tolstrup Foundation; The A.P. Møller Foundation.2017-04-042017-04-042017-04-05Bibliographically approved