Linked Life Data

21693708

Source:http://linkedlifedata.com/resource/pubmed/id/21693708

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
33
pubmed:dateCreated
2011-8-15
pubmed:abstractText
Although there is growing evidence for a role of the innate immune response in Parkinson's disease, the nature of any humoral response in dopaminergic degeneration is uncertain. Here we report on a protracted N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model of dopaminergic death that potentially allows a more full adaptive humoral response to develop. Rag2 mutant mice that lack the full adaptive response (deficient in both T and B cells) are resistant to dopaminergic death and behavioral deficiencies in this model. These mice are resensitized after reconstitution with WT splenocytes. To more directly provide evidence for humoral/IgG involvement, we show that deficiency of Fc? receptors, which are critical for activation of macrophages/microglia by binding to IgGs, is also protective in this protracted model. Fc?R-deficient mice display improved behavior and impaired microglial activation. Interestingly, however, Rag2 mutant but not Fc?R-deficient mice are resistant to a more standard N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine paradigm where death is more rapid. Taken together, these data indicate that, provided sufficient time, the humoral arm of the adaptive immune system can play a critical functional role in modulating the microglial response to dopaminergic degeneration and suggest that this humoral component may participate in degeneration in Parkinson's disease.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1083-351X
pubmed:author
pubmed:issnType
Electronic
pubmed:day
19
pubmed:volume
286
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
28783-93
pubmed:dateRevised
2011-10-19
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Involvement of the Fc gamma receptor in a chronic N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model of dopaminergic loss.
pubmed:affiliation
Department of Cellular Molecular Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't