Complement in experimental autoimmune encephalomyelitis revisited: C3 is required for development of maximal disease.
about
Lipocalin-2 protein deficiency ameliorates experimental autoimmune encephalomyelitis: the pathogenic role of lipocalin-2 in the central nervous system and peripheral lymphoid tissues.C-reactive protein-mediated vascular injury requires complement.The extracellular domain of myelin oligodendrocyte glycoprotein elicits atypical experimental autoimmune encephalomyelitis in rat and Macaque speciesActive induction of experimental autoimmune encephalomyelitis by MOG35-55 peptide immunization is associated with differential responses in separate compartments of the choroid plexusGene expression in the spinal cord in female lewis rats with experimental autoimmune encephalomyelitis induced with myelin basic proteinSuppression of cytokine-mediated complement factor gene expression through selective activation of the Ah receptor with 3',4'-dimethoxy-α-naphthoflavoneC3-dependent mechanism of microglial priming relevant to multiple sclerosis.Targeted inhibition of complement using complement receptor 2-conjugated inhibitors attenuates EAE.The integrin Mac-1 (CR3) mediates internalization and directs Bacillus anthracis spores into professional phagocytes.Therapeutic inhibition of the alternative complement pathway attenuates chronic EAE.Pathogenic and regulatory roles for B cells in experimental autoimmune encephalomyelitis.Mast cell regulation of the immune response.Enhancing the ability of experimental autoimmune encephalomyelitis to serve as a more rigorous model of multiple sclerosis through refinement of the experimental designThe complement inhibitor FUT-175 suppresses T cell autoreactivity in experimental autoimmune encephalomyelitis.Complement in multiple sclerosis: its role in disease and potential as a biomarker.Role of HLA class II genes in susceptibility and resistance to multiple sclerosis: studies using HLA transgenic miceComplement activation and expression during chronic relapsing experimental autoimmune encephalomyelitis in the Biozzi ABH mouse.Deletion of both ICAM-1 and C3 enhances severity of experimental autoimmune encephalomyelitis compared to C3-deficient miceGut dysbiosis breaks immunological tolerance toward the central nervous system during young adulthood.
P2860
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P2860
Complement in experimental autoimmune encephalomyelitis revisited: C3 is required for development of maximal disease.
description
2007 nî lūn-bûn
@nan
2007年の論文
@ja
2007年論文
@yue
2007年論文
@zh-hant
2007年論文
@zh-hk
2007年論文
@zh-mo
2007年論文
@zh-tw
2007年论文
@wuu
2007年论文
@zh
2007年论文
@zh-cn
name
Complement in experimental aut ...... evelopment of maximal disease.
@en
type
label
Complement in experimental aut ...... evelopment of maximal disease.
@en
prefLabel
Complement in experimental aut ...... evelopment of maximal disease.
@en
P2093
P2860
P1433
P1476
Complement in experimental aut ...... development of maximal disease
@en
P2093
Jillian E Adams
Scott R Barnum
Xianzhen Hu
P2860
P304
P356
10.1016/J.MOLIMM.2007.02.002
P577
2007-03-13T00:00:00Z