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- Renström, Lina, et al.
(author)
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TNF-alpha in an Overuse Muscle Model - Relationship to Muscle Fiber Necrosis/Regeneration, the NK-1 Receptor and an Occurrence of Bilateral Involvement
- 2013
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In: Journal of Clinical & Cellular Immunology. - : OMICS Publishing Group. - 2155-9899. ; 4:2
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Journal article (peer-reviewed)abstract
- TNF-alphais known to be involved in muscle damage and inflammation (myositis). Therelationships between the TNF-alpha system and muscle fibernecrosis/regeneration and the tachykinin system in this situation are unclear.We have an experimental rabbit model related to unilateral muscle overuse whichleads to marked muscle derangement and myositis bilaterally. Using this model,staining for TNF-alpha, in parallel with staining for the substance P-preferredreceptor (NK-1R) and desmin were performed. Desmin staining was used as areference concerning identification of degeneration/regeneration and the soleusmuscle was the muscle examined. It was observed that the inflammatory cells, aswell as blood vessel walls in the myositis areas, expressed TNF-alpha mRNA.Muscle fibers that were interpreted to represent necrotic fibers expressedTNF-alpha mRNA reactions and showed NK-1R immunoreactions, the reactions beingconfined to white blood cells that had infiltrated into the fibers. Musclefibers that were interpreted to be in a regenerative state expressedpatchy/widespread TNF-alpha mRNA and point like NK-1R immunoreactions. Abnormalmuscle fibers thus showed TNF-alpha mRNA as well as NK-1R immunoreactions.Normal muscle fibers never showed these reactions. Occurrence of inflammatorycell and muscle fiber TNF-alpha mRNA reactions was equally marked in the myositisareas of the contralateral side as in these areas of the ipsilateralexperimental side. The observations show that the TNF-alpha system is muchinvolved in the processes that occur in the muscle derangement/myositisprocesses. The involvement relates to effects in processes of both regenerationand muscle fiber necrosis. It may be that substance P via activation throughthe NK-1R influences the TNF-alpha expression. The findings of TNF-alphaupregulation also for the contralateral side show that the TNF-alpha system isinvolved both ipsi and contralaterally during the development of myosits/muscleaffection in response to unilateral overuse.
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| 2. |
- Andersson, Åsa, 1960-, et al.
(author)
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B-cells and Inflammation in the Absence of the Abelson Related Gene (Arg)
- 2016
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In: Journal of Clinical & Cellular Immunology. - Los Angeles, CA : Omics Publishing Group. - 2155-9899. ; 7:6
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Journal article (peer-reviewed)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.
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| 3. |
- Jacobsen, Freja A., et al.
(author)
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Arg Deficiency Does not Influence the Course of Myelin Oligodendrocyte Glycoprotein (MOG35-55)-induced Experimental Autoimmune Encephalomyelitis
- 2016
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In: Journal of Clinical & Cellular Immunology. - Los Angeles : OMICS. - 2155-9899. ; 7:3
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Journal article (peer-reviewed)abstract
- 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.
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