p150/95 (CD11c/CD18) expression is required for the development of experimental autoimmune encephalomyelitis.
about
Leukocyte integrins: role in leukocyte recruitment and as therapeutic targets in inflammatory diseaseExpression of CD11c Is Associated with Unconventional Activated T Cell Subsets with High Migratory PotentialAlpha4beta1 integrin mediates the recruitment of immature dendritic cells across the blood-brain barrier during experimental autoimmune encephalomyelitis.The complement cascade: Yin-Yang in neuroinflammation--neuro-protection and -degeneration.CD11c expression in adipose tissue and blood and its role in diet-induced obesity.Gammadelta T cells in EAE: early trafficking events and cytokine requirements.Myelin basic protein priming reduces the expression of Foxp3 in T cells via nitric oxide.Macrophages counteract demyelination in a mouse model of globoid cell leukodystrophyAbsence of β2 integrins impairs regulatory T cells and exacerbates CD4+ T cell-dependent autoimmune carditisCD11c controls herpes simplex virus 1 responses to limit virus replication during primary infection.beta2-integrins in demyelinating disease: not adhering to the paradigm.Gut mucosal injury in neonates is marked by macrophage infiltration in contrast to pleomorphic infiltrates in adult: evidence from an animal modelTargeted inhibition of complement using complement receptor 2-conjugated inhibitors attenuates EAE.IKKβ-mediated inflammatory myeloid cell activation exacerbates experimental autoimmune encephalomyelitis by potentiating Th1/Th17 cell activation and compromising blood brain barrier.Deficiency of thrombospondin-1 reduces Th17 differentiation and attenuates experimental autoimmune encephalomyelitis.Using EAE to better understand principles of immune function and autoimmune pathologyThe leucocyte β2 (CD18) integrins: the structure, functional regulation and signalling properties.Prevention of experimental cerebral malaria by Flt3 ligand during infection with Plasmodium berghei ANKA.Complement Receptors in Myeloid Cell Adhesion and Phagocytosis.Effector and suppressor roles for LFA-1 during the development of experimental autoimmune encephalomyelitis.Deletion of both ICAM-1 and C3 enhances severity of experimental autoimmune encephalomyelitis compared to C3-deficient mice
P2860
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P2860
p150/95 (CD11c/CD18) expression is required for the development of experimental autoimmune encephalomyelitis.
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
p150/95 (CD11c/CD18) expressio ...... autoimmune encephalomyelitis.
@ast
p150/95 (CD11c/CD18) expressio ...... autoimmune encephalomyelitis.
@en
type
label
p150/95 (CD11c/CD18) expressio ...... autoimmune encephalomyelitis.
@ast
p150/95 (CD11c/CD18) expressio ...... autoimmune encephalomyelitis.
@en
prefLabel
p150/95 (CD11c/CD18) expressio ...... autoimmune encephalomyelitis.
@ast
p150/95 (CD11c/CD18) expressio ...... autoimmune encephalomyelitis.
@en
P2093
P2860
P1476
p150/95 (CD11c/CD18) expressio ...... autoimmune encephalomyelitis.
@en
P2093
Daniel C Bullard
Jillian E Adams
Scott R Barnum
Trenton R Schoeb
Xianzhen Hu
P2860
P304
P356
10.2353/AJPATH.2007.061016
P407
P577
2007-06-01T00:00:00Z