TY - JOUR
AU - 
AB - <jats:title>Abstract</jats:title>
               <jats:p>Macrophages and microglia are central players in the pathogenesis of inflammatory diseases in the CNS, such as Multiple Sclerosis. SOCS proteins are critical feedback inhibitors of the JAK/STAT pathway, and negatively regulate innate and adaptive immune responses. Our Previous Studies indicated that SOCS3 is a negative regulator of macrophage and microglia activation. Experimental autoimmune encephalomyelitis (EAE), an animal model of MS, is used to study the function of SOCS3 in neuroinflammation. Mice with conditional SOCS3 deletion in myeloid lineage cells (LysMCreSOCS3fl/fl) were generated from SOCS3fl/fl mice. Our results indicated that LysMCreSOCS3fl/fl mice are remarkably vulnerable to MOG-induced EAE, with features characteristic of atypical EAE, an earlier onset and more severe of EAE than SOCS3fl/fl mice. The lack of SOCS3 in myeloid lineage cells led to enhanced infiltration of inflammatory cells and enhanced demyelination in the cerebellum, and expression of inflammatory cytokines and chemokines in the cerebellum, and an immune response dominated by Th1 cells. Furthermore, the adoptive transfer experiments demonstrated that macrophage with SOCS3 expression rescues LysMCreSOCS3fl/fl mice from atypical EAE by inhibition of IFN-γ, IL-6, CCL2 and CXCL10 expression. Our study suggests that SOCS3 is a critical negative regulator in EAE pathogenesis, specifically in the development of atypical EAE. SOCS3 may service as an approach to new therapeutics for MS patients.</jats:p>
TI - Critical function of myeloid SOCS3 is in limiting the neuroinflammation of EAE (147.21)
JO - The Journal of Immunology
DO - 10.4049/jimmunol.186.supp.147.21
DA - 2011-04-01
UR - https://www.deepdyve.com/lp/crossref/critical-function-of-myeloid-socs3-is-in-limiting-the-ry1e9M0m68
SP - 147.21
EP - 147.21
VL - 186
IS - 1_Supplement
DP - DeepDyve
ER -