scholarly journals Upregulation and coexpression of adhesion molecules correlate with relapsing autoimmune demyelination in the central nervous system.

1990 ◽  
Vol 172 (5) ◽  
pp. 1521-1524 ◽  
Author(s):  
B Cannella ◽  
A H Cross ◽  
C S Raine
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Adhesion Molecules ◽  
Cell Invasion ◽  
Inflammatory Cell ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Murine Homologue ◽  
The Central Nervous System ◽  
Autoimmune Demyelination

The expression of adhesion molecules on central nervous system (CNS) vessels was examined during chronic relapsing experimental autoimmune encephalomyelitis in the SJL mouse. Two molecules associated with cell adhesion were studied: MECA-325, a murine lymph node high endothelial venule marker; and MALA-2, the murine homologue of intercellular adhesion molecule 1. During initial disease, upregulated coexpression of these two molecules occurred in the CNS. This correlated with inflammatory cell invasion. During remission, expression was downregulated, and each subsequent relapse was accompanied by corresponding upregulation. Thus, up- and downregulation of adhesion molecules in the target organ appeared to form an integral part of the inflammatory process in this autoimmune condition and support a role for receptor-mediated inflammatory cell invasion of relevance to the pathogenesis of multiple sclerosis.

scholarly journals Olfactory Ensheathing Glia: Drivers of Axonal Regeneration in the Central Nervous System?

2002 ◽  
Vol 2 (1) ◽  
pp. 37-43 ◽  
Author(s):  
M. Teresa Moreno-Flores ◽  
Javier Díaz-Nido ◽  
Francisco Wandosell ◽  
Jesús Avila
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Adhesion Molecules ◽  
Neurotrophic Factors ◽  
Axonal Regeneration ◽  
Cns Regeneration ◽  
The Central Nervous System ◽  
Large Heterogeneity ◽  
Olfactory Ensheathing Glia ◽  
Glial Scarring

Olfactory ensheathing glia (OEG) accompany olfactory growing axons in their entry to the adult mammalian central nervous system (CNS). Due to this special characteristic, considerable attention has been focused on the possibility of using OEG for CNS regeneration. OEG present a large heterogeneity in culture with respect to their cellular morphology and expressed molecules. The specific characteristics of OEG responsible for their regenerative properties have to be defined. These properties probably result from the combination of several factors: molecular composition of the membrane (expressing adhesion molecules as PSA-NCAM, L1 and/or others) combined with their ability to reduce glial scarring and to accompany new growing axons into the host CNS. Their capacity to produce some neurotrophic factors might also account for their ability to produce CNS regeneration.

scholarly journals Chemokines Referee Inflammation within the Central Nervous System during Infection and Disease

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Douglas M. Durrant ◽  
Jessica L. Williams ◽  
Brian P. Daniels ◽  
Robyn S. Klein
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Essential Role ◽  
Inflammatory Cell ◽  
Cell Types ◽  
Effector Molecules ◽  
The Past ◽  
Inflammatory Conditions ◽  
Endothelial Barriers ◽  
The Central Nervous System

The discovery that chemokines and their receptors are expressed by a variety of cell types within the normal adult central nervous system (CNS) has led to an expansion of their repertoire as molecular interfaces between the immune and nervous systems. Thus, CNS chemokines are now divided into those molecules that regulate inflammatory cell migration into the CNS and those that initiate CNS repair from inflammation-mediated tissue damage. Work in our laboratory throughout the past decade has sought to elucidate how chemokines coordinate leukocyte entry and interactions at CNS endothelial barriers, under both homeostatic and inflammatory conditions, and how they promote repair within the CNS parenchyma. These studies have identified several chemokines, including CXCL12 and CXCL10, as critical regulators of leukocyte migration from perivascular locations. CXCL12 additionally plays an essential role in promoting remyelination of injured white matter. In both scenarios we have shown that chemokines serve as molecular links between inflammatory mediators and other effector molecules involved in neuroprotective processes.

scholarly journals The Th17–ELR+ CXC chemokine pathway is essential for the development of central nervous system autoimmune disease

2008 ◽  
Vol 205 (4) ◽  
pp. 811-823 ◽  
Author(s):  
Thaddeus Carlson ◽  
Mark Kroenke ◽  
Praveen Rao ◽  
Thomas E. Lane ◽  
Benjamin Segal
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Th17 Cells ◽  
Polymorphonuclear Leukocytes ◽  
Autoimmune Encephalomyelitis ◽  
Cxc Chemokine ◽  
The Central Nervous System ◽  
Autoimmune Demyelination ◽  
Clinical Deficits ◽  
Experimental Autoimmune

The ELR+ CXC chemokines CXCL1 and CXCL2 are up-regulated in the central nervous system (CNS) during multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). However, their functional significance and the pathways regulating their expression are largely unknown. We show that transfer of encephalitogenic CD4+ Th17 cells is sufficient to induce CXCL1 and CXCL2 transcription in the spinal cords of naive, syngeneic recipients. Blockade or genetic silencing of CXCR2, a major receptor for these chemokines in mice, abrogates blood–brain barrier (BBB) breakdown, CNS infiltration by leukocytes, and the development of clinical deficits during the presentation as well as relapses of EAE. Depletion of circulating polymorphonuclear leukocytes (PMN) had a similar therapeutic effect. Furthermore, injection of CXCR2+ PMN into CXCR2−/− mice was sufficient to restore susceptibility to EAE. Our findings reveal that a Th17–ELR+ CXC chemokine pathway is critical for granulocyte mobilization, BBB compromise, and the clinical manifestation of autoimmune demyelination in myelin peptide–sensitized mice, and suggest new therapeutic targets for diseases such as MS.

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