scholarly journals Activation of Invariant NKT Cells in Early Phase of Experimental Autoimmune Encephalomyelitis Results in Differentiation of Ly6ChiInflammatory Monocyte to M2 Macrophages and Improved Outcome

2012 ◽  
Vol 189 (2) ◽  
pp. 551-557 ◽  
Author(s):  
Laura Denney ◽  
Wai Ling Kok ◽  
Suzanne L. Cole ◽  
Sharon Sanderson ◽  
Andrew J. McMichael ◽  
...  
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Early Phase ◽  
Nkt Cells ◽  
M2 Macrophages ◽  
Autoimmune Encephalomyelitis ◽  
Invariant Nkt Cells ◽  
Improved Outcome ◽  
Experimental Autoimmune

scholarly journals Targeting the Shift from M1 to M2 Macrophages in Experimental Autoimmune Encephalomyelitis Mice Treated with Fasudil

PLoS ONE ◽  
2013 ◽  
Vol 8 (2) ◽  
pp. e54841 ◽  
Author(s):  
Chunyun Liu ◽  
Yanhua Li ◽  
Jiezhong Yu ◽  
Ling Feng ◽  
Shaowei Hou ◽  
...  
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
M2 Macrophages ◽  
Autoimmune Encephalomyelitis ◽  
Experimental Autoimmune

scholarly journals Natural Killer T Cell Activation Protects Mice Against Experimental Autoimmune Encephalomyelitis

2001 ◽  
Vol 194 (12) ◽  
pp. 1801-1811 ◽  
Author(s):  
Avneesh K. Singh ◽  
Michael T. Wilson ◽  
Seokmann Hong ◽  
Danyvid Olivares-Villagómez ◽  
Caigan Du ◽  
...  
Keyword(s):  
T Cell ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Natural Killer ◽  
Critical Role ◽  
Nkt Cells ◽  
Target Cells ◽  
Autoimmune Encephalomyelitis ◽  
Presentation Pathway ◽  
Experimental Autoimmune ◽  
Natural Killer T

Experimental autoimmune encephalomyelitis (EAE) serves as a prototypic model for T cell–mediated autoimmunity. Vα14 natural killer T (NKT) cells are a subset of T lymphocytes that recognize glycolipid antigens presented by the nonpolymorphic major histocompatibility complex (MHC) class I–like protein CD1d. Here, we show that activation of Vα14 NKT cells by the glycosphingolipid α-galactosylceramide (α-GalCer) protects susceptible mice against EAE. β-GalCer, which binds CD1d but is not recognized by NKT cells, failed to protect mice against EAE. Furthermore, α-GalCer was unable to protect CD1d knockout (KO) mice against EAE, indicating the requirement for an intact CD1d antigen presentation pathway. Protection of disease conferred by α-GalCer correlated with its ability to suppress myelin antigen-specific Th1 responses and/or to promote myelin antigen-specific Th2 cell responses. α-GalCer was unable to protect IL-4 KO and IL-10 KO mice against EAE, indicating a critical role for both of these cytokines. Because recognition of α-GalCer by NKT cells is phylogenetically conserved, our findings have identified NKT cells as novel target cells for treatment of inflammatory diseases of the central nervous system.

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