NDLI: P2x7 deficiency suppresses development of experimental autoimmune encephalomyelitis

Content Provider	Springer Nature : BioMed Central
Author	Sharp, Anthony J Polak, Paul E Simonini, Vittoria Lin, Shao X Richardson, Jill C Bongarzone, Ernesto R Feinstein, Douglas L
Abstract	Background The purinergic receptor P2x7 is expressed on myeloid cells as well as on CNS glial cells, and P2x7 activation has been shown to increase both glial and T-cell activation. These properties suggest a role in the development of autoimmune disease including multiple sclerosis. Methods The animal model of MS, experimental autoimmune encephalomyelitis (EAE) using myelin oligodendrocyte glycoprotein (MOG) peptide residues 35–55 was induced in wildtype C57BL6 mice and in P2x7 deficient mice ('P2x7 mice') that were backcrossed to C57BL6 mice. Disease progression was monitored by appearance of clinical signs, immunocytochemical staining to assess brain inflammation and neuronal damage, and by measurement of Tcell cytokine production. Results The incidence of EAE disease in P2x7 mice was reduced 4-fold compared to the wildtype mice; however the P2x7 mice that became ill had similar days of onset and clinical scores as the wildtype mice. Splenic T-cells isolated from P2x7 null mice produced greater IFNγ and IL-17 (from 3 to 12 fold greater levels) than wildtype cells, however cytokine production from P2x7 derived cells was not increased by a selective P2x7 agonist as was cytokine production from wildtype cells. Although infiltrating cells were detected in brains of both the P2x7 and wildtype mice, astroglial activation and axonal damage was reduced versus wildtype mice, and the distribution of astroglial activation was markedly distinct in the two strains. In contrast, microglial activation was similar in the two strains. Conclusion P2x7 deficiency resulted in compensatory changes leading to increased T-cell cytokine production, and activated T-cells were detected in the brains of P2x7 null mice with no clinical signs. However, the greatly reduced incidence of disease suggests that an initiating event is absent in these mice, and points to a role for astroglial P2x7 in development of EAE disease.
Related Links	https://jneuroinflammation.biomedcentral.com/counter/pdf/10.1186/1742-2094-5-33.pdf
Ending Page	13
Page Count	13
Starting Page	1
File Format	HTM / HTML
ISSN	17422094
DOI	10.1186/1742-2094-5-33
Journal	Journal of Neuroinflammation
Issue Number	1
Volume Number	5
Language	English
Publisher	BioMed Central
Publisher Date	2008-08-08
Access Restriction	Open
Subject Keyword	Neurosciences Neurology Neurobiology Immunology Experimental Autoimmune Encephalomyelitis Myelin Oligodendrocyte Glycoprotein Experimental Autoimmune Encephalomyelitis Mouse Wildtype Mouse Astroglial Activation
Content Type	Text
Resource Type	Article
Subject	Neuroscience Immunology Cellular and Molecular Neuroscience Neurology
Journal Impact Factor	9.3/2023
5-Year Journal Impact Factor	9.8/2023

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Predominance of Th2 polarization by Vitamin D through a STAT6-dependent mechanism

Greatly attenuated experimental autoimmune encephalomyelitis in aquaporin-4 knockout mice

Amelioration of autoimmune neuroinflammation by the fusion molecule Fn14·TRAIL

Alterations of peripheral nerve excitability in an experimental autoimmune encephalomyelitis mouse model for multiple sclerosis

P2x7 deficiency suppresses development of experimental autoimmune encephalomyelitis

15d-PGJ2 induces apoptosis of mouse oligodendrocyte precursor cells

Loss of the receptor tyrosine kinase Axl leads to enhanced inflammation in the CNS and delayed removal of myelin debris during Experimental Autoimmune Encephalomyelitis

CX3CL1 (fractalkine) and CX3CR1 expression in myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis: kinetics and cellular origin

Chronic immobilisation stress ameliorates clinical score and neuroinflammation in a MOG-induced EAE in Dark Agouti rats: mechanisms implicated

P2x7 deficiency suppresses development of experimental autoimmune encephalomyelitis

Similar Documents

Predominance of Th2 polarization by Vitamin D through a STAT6-dependent mechanism

Greatly attenuated experimental autoimmune encephalomyelitis in aquaporin-4 knockout mice

Amelioration of autoimmune neuroinflammation by the fusion molecule Fn14·TRAIL

Alterations of peripheral nerve excitability in an experimental autoimmune encephalomyelitis mouse model for multiple sclerosis

P2x7 deficiency suppresses development of experimental autoimmune encephalomyelitis

15d-PGJ2 induces apoptosis of mouse oligodendrocyte precursor cells

Loss of the receptor tyrosine kinase Axl leads to enhanced inflammation in the CNS and delayed removal of myelin debris during Experimental Autoimmune Encephalomyelitis

CX3CL1 (fractalkine) and CX3CR1 expression in myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis: kinetics and cellular origin

Chronic immobilisation stress ameliorates clinical score and neuroinflammation in a MOG-induced EAE in Dark Agouti rats: mechanisms implicated

P2x7 deficiency suppresses development of experimental autoimmune encephalomyelitis