Fast Progression of Recombinant Human Myelin/Oligodendrocyte Glycoprotein (MOG)-Induced Experimental Autoimmune Encephalomyelitis in Marmosets Is Associated with the Activation of MOG34-56-Specific Cytotoxic T Cells.

Fast Progression of Recombinant Human Myelin/Oligodendrocyte Glycoprotein (MOG)-Induced Experimental Autoimmune Encephalomyelitis in Marmosets Is Associated with the Activation of MOG34-56-Specific Cytotoxic T Cells. Research Abstract Details 

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Fast Progression of Recombinant Human Myelin/Oligodendrocyte Glycoprotein (MOG)-Induced Experimental Autoimmune Encephalomyelitis in Marmosets Is Associated with the Activation of MOG34-56-Specific Cytotoxic T Cells. Abstract Text:

Yolanda S Kap,Paul Smith,S Anwar Jagessar,Ed Remarque,Erwin Blezer,Gustav J Strijkers,Jon D Laman,Rogier Q Hintzen,Jan Bauer,Herbert P M Brok,Bert A 't Hart,Yolanda S Kap,Paul Smith,S Anwar Jagessar,Ed Remarque,Erwin Blezer,Gustav J Strijkers,Jon D Laman,Rogier Q Hintzen,Jan Bauer,Herbert P M Brok,Bert A 't Hart,

The recombinant human (rh) myelin/oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) model in the common marmoset is characterized by 100% disease incidence, a chronic disease course, and a variable time interval between immunization and neurological impairment. We investigated whether monkeys with fast and slow disease progression display different anti-MOG T or B cell responses and analyzed the underlying pathogenic mechanism(s). The results show that fast progressor monkeys display a significantly wider specificity diversification of anti-MOG T cells at necropsy than slow progressors, especially against MOG(34-56) and MOG(74-96). MOG(34-56) emerged as a critical encephalitogenic peptide, inducing severe neurological disease and multiple lesions with inflammation, demyelination, and axonal injury in the CNS. Although EAE was not observed in MOG(74-96)-immunized monkeys, weak T cell responses against MOG(34-56) and low grade CNS pathology were detected. When these cases received a booster immunization with MOG(34-56) in IFA, full-blown EAE developed. MOG(34-56)-reactive T cells expressed CD3, CD4, or CD8 and CD56, but not CD16. Moreover, MOG(34-56)-specific T cell lines displayed specific cytotoxic activity against peptide-pulsed B cell lines. The phenotype and cytotoxic activity suggest that these cells are NK-CTL. These results support the concept that cytotoxic cells may play a role in the pathogenesis of multiple sclerosis.

Fast Progression of Recombinant Human Myelin/Oligodendrocyte Glycoprotein (MOG)-Induced Experimental Autoimmune Encephalomyelitis in Marmosets Is Associated with the Activation of MOG34-56-Specific Cytotoxic T Cells. Publishing Authors By Initials

YS Kap,P Smith,SA Jagessar,E Remarque,E Blezer,GJ Strijkers,JD Laman,RQ Hintzen,J Bauer,HP Brok,BA 't Hart,YS Kap,P Smith,SA Jagessar,E Remarque,E Blezer,GJ Strijkers,JD Laman,RQ Hintzen,J Bauer,HP Brok,BA 't Hart,

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Fast Progression of Recombinant Human Myelin/Oligodendrocyte Glycoprotein (MOG)-Induced Experimental Autoimmune Encephalomyelitis in Marmosets Is Associated with the Activation of MOG34-56-Specific Cytotoxic T Cells. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Journal of immunology (Baltimore, Md. : 1950)

VOLUME: 180

Page Numbers: 1326-37

Journal Abbreviation: J. Immunol.

ISSN: 0022-1767

DAY: 1

MONTH: Feb

YEAR: 2008

Fast Progression of Recombinant Human Myelin/Oligodendrocyte Glycoprotein (MOG)-Induced Experimental Autoimmune Encephalomyelitis in Marmosets Is Associated with the Activation of MOG34-56-Specific Cytotoxic T Cells. Information

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LANGUAGE: eng

NlmUniqueID: 2985117

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AFFILIATION: Department of Immunobiology.

Country: United States

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MEDLINETA: J Immunol

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