NDLI: GM-CSF-neuroantigen fusion proteins reverse experimental autoimmune encephalomyelitis and mediate tolerogenic activity in adjuvant-primed environments: association with inflammation-dependent, inhibitory antigen presentation.

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GM-CSF-neuroantigen fusion proteins reverse experimental autoimmune encephalomyelitis and mediate tolerogenic activity in adjuvant-primed environments: association with inflammation-dependent, inhibitory antigen presentation.

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GM-CSF-neuroantigen fusion proteins reverse experimental autoimmune encephalomyelitis and mediate tolerogenic activity in adjuvant-primed environments: association with inflammation-dependent, inhibitory antigen presentation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Islam, S. M. Touhidul Wilkinson, Daniel S. Taslim, Najla Mannie, Mark D. Curtis, Alan D.
Description	Author Affiliation: Islam SM ( Department of Microbiology and Immunology, Brody School of Medicine, East Carolina University, Greenville, NC 27834.); Curtis AD ( Department of Microbiology and Immunology, Brody School of Medicine, East Carolina University, Greenville, NC 27834.); Taslim N ( Department of Microbiology and Immunology, Brody School of Medicine, East Carolina University, Greenville, NC 27834.); Wilkinson DS ( Department of Microbiology and Immunology, Brody School of Medicine, East Carolina University, Greenville, NC 27834.); Mannie MD ( Department of Microbiology and Immunology, Brody School of Medicine, East Carolina University, Greenville, NC 27834 manniem@ecu.edu.)
Abstract	Single-chain fusion proteins comprised of GM-CSF and neuroantigen (NAg) are potent, NAg-specific inhibitors of experimental autoimmune encephalomyelitis (EAE). An important question was whether GMCSF-NAg tolerogenic vaccines retained inhibitory activity within inflammatory environments or were contingent upon steady-state conditions. GM-CSF fused to the myelin oligodendrocyte glycoprotein MOG35-55 peptide (GMCSF-MOG) reversed established paralytic disease in both passive and active models of EAE in C57BL/6 mice. The fusion protein also reversed EAE in CD4-deficient and B cell-deficient mice. Notably, GMCSF-MOG inhibited EAE when coinjected adjacent to the MOG35-55/CFA emulsion. GMCSF-MOG also retained dominant inhibitory activity when directly emulsified with MOG35-55 in the CFA emulsion in both C57BL/6 or B cell-deficient models of EAE. Likewise, when combined with proteolipid protein 139-151 in CFA, GM-CSF fused to proteolipid protein 139-151 peptide inhibited EAE in SJL mice. When deliberately emulsified in CFA with the NAg, GMCSF-NAg inhibited EAE even though NAg was present at >30-fold molar excess. In vitro studies revealed that the GM-CSF domain of GMCSF-MOG stimulated growth and differentiation of inflammatory dendritic cells (DC) and simultaneously targeted the MOG35-55 domain for enhanced presentation by these DC. These inflammatory DC presented MOG35-55 to MOG-specific T cells by an inhibitory mechanism that was mediated in part by IFN-Î³ signaling and NO production. In conclusion, GMCSF-NAg was tolerogenic in CFA-primed proinflammatory environments by a mechanism associated with targeted Ag presentation by inflammatory DC and an inhibitory IFN-Î³/NO pathway. The inhibitory activity of GMCSF-NAg in CFA-primed lymphatics distinguishes GMCSF-NAg fusion proteins as a unique class of inflammation-dependent tolerogens that are mechanistically distinct from naked peptide or protein-based tolerogens.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1303223
Journal	The Journal of Immunology
Issue Number	5
Volume Number	193
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-09-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Antigen Presentation Drug Effects Autoantigens Pharmacology Encephalomyelitis, Autoimmune, Experimental Drug Therapy Granulocyte-macrophage Colony-stimulating Factor Immune Tolerance Myelin-oligodendrocyte Glycoprotein Animals Genetics Immunology Pathology Inflammation Interferon-gamma Mice Nitric Oxide Peptide Fragments Recombinant Fusion Proteins Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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