Journal
CLINICAL IMMUNOLOGY
Volume 197, Issue -, Pages 45-53Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.clim.2018.08.006
Keywords
Multiple sclerosis; Experimental autoimmune encephalomyelitis; IL-11; Th17 cells; Demyelination; Diffusion Tensor Imaging
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Funding
- National Center for Advancing Translational Sciences (NCATS), National Institutes of Health [UL1TR001111]
- NCI [2-P30-CA016086-40]
- NIEHS [2-P30ES010126-15A1]
- UCRF
- NCBT [2015-IDG-1007]
- Cancer Center Core Support Grant [P30 CA016086]
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IL-11 induced differentiation and expansion of Th17 cells in patients with early relapsing-remitting multiple sclerosis (RRMS). In mice with relapsing-remitting experimental autoimmune encephalomyelitis (RREAE), IL-11 exacerbated disease, induced demyelination in the central nervous system (CNS), increased the percentage of IL-17A(+) CD4(+) Th17 cells in the CNS in the early acute phase, and up-regulated serum IL-17A levels and the percentage of IL-17A(+) CD4(+) Th17 cells in lymph nodes, and IFN-gamma(+)CD4(+) T cells in spinal cord in the RR phase. IL-11 antagonist suppressed RREAE disease activities, inhibited IL-17A(+)CD4(+) cell infiltration and demyelination in the CNS, and decreased the percentage of IL-17A(+) CD4(+) T cells in peripheral blood mononuclear cells and ICAM1(+) CD4(+) T cells in brain and SC. Diffusion Tensor Imaging indicated that IL-11 antagonist inhibited demyelination in several brain regions. We conclude that by suppressing Th17 cell-mediated neuroinflammation and demyelination, IL-11 antagonist can be further studied as a potential selective and early therapy for RRMS.
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