Melatonin enhances interleukin-10 expression and suppresses chemotaxis to inhibit inflammation in situ and reduce the severity of experimental autoimmune encephalomyelitis

2016 ◽  
Vol 31 ◽  
pp. 169-177 ◽  
Author(s):  
Shyi-Jou Chen ◽  
Shing-Hwa Huang ◽  
Jing-Wun Chen ◽  
Kai-Chen Wang ◽  
Yung-Rong Yang ◽  
...  
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Interleukin 10 ◽  
Autoimmune Encephalomyelitis ◽  
Experimental Autoimmune

scholarly journals Induction of Golli-MBP Expression in CNS Macrophages During Acute LPS-Induced CNS Inflammation and Experimental Autoimmune Encephalomyelitis (EAE)

2007 ◽  
Vol 7 ◽  
pp. 112-120 ◽  
Author(s):  
Tracey L. Papenfuss ◽  
J. Cameron Thrash ◽  
Patricia E. Danielson ◽  
Pamela E. Foye ◽  
Brian S. Hllbrush ◽  
...  
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Cell Type ◽  
Autoimmune Encephalomyelitis ◽  
Cns Inflammation ◽  
Cell Type Specific ◽  
Candidate Molecule ◽  
Experimental Autoimmune

Microglia are the tissue macrophages of the CNS. Microglial activation coupled with macrophage infiltration is a common feature of many classic neurodegenerative disorders. The absence of cell-type specific markers has confounded and complicated the analysis of cell-type specific contributions toward the onset, progression, and remission of neurodegeneration. Molecular screens comparing gene expression in cultured microglia and macrophages identified Golli-myelin basic protein (MBP) as a candidate molecule enriched in peripheral macrophages.In situhybridization analysis of LPS/IFNg and experimental autoimmune encephalomyelitis (EAE)–induced CNS inflammation revealed that only a subset of CNS macrophages express Golli-MBP. Interestingly, the location and morphology of Golli-MBP+ CNS macrophages differs between these two models of CNS inflammation. These data demonstrate the difficulties of extendingin vitroobservations toin vivobiology and concretely illustrate the complex heterogeneity of macrophage activation states present in region- and stage-specific phases of CNS inflammation. Taken altogether, these are consistent with the emerging picture that the phenotype of CNS macrophages is actively defined by their molecular interactions with the CNS microenvironment.

scholarly journals Transgenic Interleukin 10 Prevents Induction of Experimental Autoimmune Encephalomyelitis

1999 ◽  
Vol 189 (6) ◽  
pp. 1005-1010 ◽  
Author(s):  
Daniel J. Cua ◽  
Herve Groux ◽  
David R. Hinton ◽  
Stephen A. Stohlman ◽  
Robert L. Coffman
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Transgenic Mice ◽  
Mhc Class Ii ◽  
Cell Function ◽  
Class Ii ◽  
Interleukin 10 ◽  
T Helper 1 ◽  
Autoimmune Encephalomyelitis ◽  
Autoreactive T Cell ◽  
Experimental Autoimmune

The effectiveness of interleukin 10 (IL-10) in the treatment of autoimmune-mediated central nervous system inflammation is controversial. Studies of the model system, experimental autoimmune encephalomyelitis (EAE), using various routes, regimens, and delivery methods of IL-10 suggest that these variables may affect its immunoregulatory function. To study the influence of these factors on IL-10 regulation of EAE pathogenesis, we have analyzed transgenic mice expressing human IL-10 (hIL-10) transgene under the control of a class II major histocompatibility complex (MHC) promoter. The hIL-10 transgenic mice are highly resistant to EAE induced by active immunization, and this resistance appears to be mediated by suppression of autoreactive T cell function. Myelin-reactive T helper 1 cells are induced but nonpathogenic in the IL-10 transgenic mice. Antibody depletion confirmed that EAE resistance is dependent on the presence of the transgenic IL-10. Mice expressing the hIL-10 transgene but not the endogenous murine IL-10 gene demonstrated that transgenic IL-10 from MHC class II–expressing cells is sufficient to block induction of EAE. This study demonstrates that IL-10 can prevent EAE completely if present at appropriate levels and times during disease induction.

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