| Content Provider |
World Health Organization (WHO)-Global Index Medicus |
| Author |
Russell, John H. Parker Harp, Chelsea R. Ferris, Stephen T. Archambault, Angela S. Sim, Julia Koni, Pandelakis A. Wu, Gregory F. Mikesell, Robert J. Linington, Christopher Shimoda, Michiko |
| Description |
Author Affiliation: Parker Harp CR ( Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110); Archambault AS ( Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110); Sim J ( Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110); Ferris ST ( Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110); Mikesell RJ ( Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110); Koni PA ( Cancer Immunology, Inflammation, and Tolerance Program, Cancer Center and Department of Medicine, Georgia Regents University, Augusta, GA 30912); Shimoda M ( Department of Dermatology, University of California at Davis School of Medicine, Sacramento, CA 95817); Linington C ( Department of Immunology, University of Glasgow, Glasgow G12 8QQ, United Kingdom.); Russell JH ( Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110); Wu GF ( Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110) |
| Abstract |
B cells are increasingly regarded as integral to the pathogenesis of multiple sclerosis, in part as a result of the success of B cell-depletion therapy. Multiple B cell-dependent mechanisms contributing to inflammatory demyelination of the CNS have been explored using experimental autoimmune encephalomyelitis (EAE), a CD4 T cell-dependent animal model for multiple sclerosis. Although B cell Ag presentation was suggested to regulate CNS inflammation during EAE, direct evidence that B cells can independently support Ag-specific autoimmune responses by CD4 T cells in EAE is lacking. Using a newly developed murine model of in vivo conditional expression of MHC class II, we reported previously that encephalitogenic CD4 T cells are incapable of inducing EAE when B cells are the sole APC. In this study, we find that B cells cooperate with dendritic cells to enhance EAE severity resulting from myelin oligodendrocyte glycoprotein (MOG) immunization. Further, increasing the precursor frequency of MOG-specific B cells, but not the addition of soluble MOG-specific Ab, is sufficient to drive EAE in mice expressing MHCII by B cells alone. These data support a model in which expansion of Ag-specific B cells during CNS autoimmunity amplifies cognate interactions between B and CD4 T cells and have the capacity to independently drive neuroinflammation at later stages of disease. |
| ISSN |
00221767 |
| e-ISSN |
15506606 |
| DOI |
10.4049/jimmunol.1402236 |
| Journal |
The Journal of Immunology |
| Issue Number |
11 |
| Volume Number |
194 |
| Language |
English |
| Publisher |
The American Association of Immunologists |
| Publisher Date |
2015-06-01 |
| Publisher Place |
United States |
| Access Restriction |
Open |
| Subject Keyword |
Antigen Presentation Immunology B-lymphocytes Encephalomyelitis, Autoimmune, Experimental Multiple Sclerosis Myelin-oligodendrocyte Glycoprotein Neurogenic Inflammation Animals Cd4-positive T-lymphocytes Dendritic Cells Pathology Histocompatibility Antigens Class Ii Biosynthesis Mice Mice, Inbred C57bl Administration & Dosage Research Support, N.i.h., Extramural Discipline Immunology |
| Content Type |
Text |
| Resource Type |
Article |
| Subject |
Immunology and Allergy Immunology |
