Up-regulation of major histocompatibility complex class II antigen expression in the central nervous system of dogs with spontaneous canine distemper virus encephalitis

1996 ◽  
Vol 92 (3) ◽  
pp. 273-280 ◽  
Author(s):  
S. Alldinger ◽  
A. Wünschmann ◽  
W. Baumgärtner ◽  
C. Voss ◽  
E. Kremmer
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Major Histocompatibility Complex ◽  
Canine Distemper Virus ◽  
Antigen Expression ◽  
Complex Class ◽  
Canine Distemper ◽  
Histocompatibility Complex ◽  
The Central Nervous System ◽  
Class Ii Antigen

scholarly journals The nervous form of canine distemper

2018 ◽  
Vol 13 (2) ◽  
pp. 125-136
Author(s):  
Alice Fernandes Alfieri ◽  
Alexandre Mendes Amude ◽  
Amauri Alcindo Alfier
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Canine Distemper Virus ◽  
Demyelinating Disease ◽  
Clinical Course ◽  
Systemic Infection ◽  
Canine Distemper ◽  
Systemic Involvement ◽  
Clinical Syndromes ◽  
The Central Nervous System

Canine distemper is a systemic infection, frequently lethal in dogs. The canine distemper virus(CDV) causes a persistent infection within the central nervous system resulting in aprogressive, multifocal demyelinating disease. In dogs, CDV infection may lead togastrointestinal and/or respiratory signs, frequently with central nervous system involvement.Myoclonus has been a common and characteristic sign observed in dogs with distemperencephalomyelitis. However, the nervous form of distemper may occur in the absence ofmyoclonus and systemic involvement. This review will point the clinical course and theneurological signs of nervous distemper, as well the clinical syndromes of CDV infection,neuropathology of acute and chronic demyelination, and diagnostic aids of CDVencephalomyelitis.

scholarly journals Extracellular histone H1 is neurotoxic and drives a pro-inflammatory response in microglia

F1000Research ◽  
2013 ◽  
Vol 2 ◽  
pp. 148 ◽  
Author(s):  
Jonathan D Gilthorpe ◽  
Fazal Oozeer ◽  
Julia Nash ◽  
Margarita Calvo ◽  
David LH Bennett ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Mhc Class Ii ◽  
Cortical Neurons ◽  
Antigen Expression ◽  
Histone H1 ◽  
Adult Brain ◽  
Core Histones ◽  
The Central Nervous System ◽  
Class Ii Antigen

In neurodegenerative conditions and following brain trauma it is not understood why neurons die while astrocytes and microglia survive and adopt pro-inflammatory phenotypes. We show here that the damaged adult brain releases diffusible factors that can kill cortical neurons and we have identified histone H1 as a major extracellular candidate that causes neurotoxicity and activation of the innate immune system. Extracellular core histones H2A, H2B H3 and H4 were not neurotoxic. Innate immunity in the central nervous system is mediated through microglial cells and we show here for the first time that histone H1 promotes their survival, up-regulates MHC class II antigen expression and is a powerful microglial chemoattractant. We propose that when the central nervous system is degenerating, histone H1 drives a positive feedback loop that drives further degeneration and activation of immune defences which can themselves be damaging. We suggest that histone H1 acts as an antimicrobial peptide and kills neurons through mitochondrial damage and apoptosis.

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