Linked Life Data

19850104

Source:http://linkedlifedata.com/resource/pubmed/id/19850104

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2009-11-16
pubmed:abstractText
Multiple sclerosis (MS) is an autoimmune disease in which inflammation, leukocyte infiltration, and ultimately, demyelination occur as a result of innate and adaptive immune-mediated mechanisms. The pathophysiological role of the complement system, a major component of innate immunity, in the development and progression of experimental autoimmune encephalomyelitis (EAE), the animal model for MS has been extensively examined. Previous studies from our lab have shown that the complement receptor for the anaphylatoxin C3a, but not for C5a plays an important role in EAE. Based on the important contributions of the complement anaphylatoxin receptors to other inflammatory conditions in the CNS, we reasoned that deletion of both receptors may reveal underlying interactions between them that are important to EAE pathology. We performed EAE in C3aR/C5aR double knockout mice (C3aR/C5aR(-/-)) and observed delayed onset of disease but no attenuation of disease severity compared to wild type mice. Interestingly there was trend toward greater infiltration of CD4(+), but not CD8(+) T cells, in C3aR/C5aR(-/-) mice with EAE, suggesting altered trafficking of these cells. Antigen-specific T cells isolated from C3aR/C5aR(-/-) mice during acute EAE produced elevated levels of TNF-alpha, but markedly reduced levels of IFN-gamma and IL-12 compared to wild type mice. It remains unclear how the changes in these disease parameters contribute to the loss of the protective effect seen in C3aR(-/-) mice, however our data indicate a level of cross-modulation between the C3aR and C5aR during EAE.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1872-7972
pubmed:author
pubmed:issnType
Electronic
pubmed:day
31
pubmed:volume
467
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
234-6
pubmed:dateRevised
2011-6-7
pubmed:meshHeading
pubmed-meshheading:19850104-Animals, pubmed-meshheading:19850104-CD4-Positive T-Lymphocytes, pubmed-meshheading:19850104-Cell Movement, pubmed-meshheading:19850104-Complement C3a, pubmed-meshheading:19850104-Cytokines, pubmed-meshheading:19850104-Disease Models, Animal, pubmed-meshheading:19850104-Encephalomyelitis, Autoimmune, Experimental, pubmed-meshheading:19850104-Female, pubmed-meshheading:19850104-Gene Deletion, pubmed-meshheading:19850104-Genetic Predisposition to Disease, pubmed-meshheading:19850104-Male, pubmed-meshheading:19850104-Mice, pubmed-meshheading:19850104-Mice, Inbred C57BL, pubmed-meshheading:19850104-Mice, Knockout, pubmed-meshheading:19850104-Multiple Sclerosis, pubmed-meshheading:19850104-Receptor, Anaphylatoxin C5a, pubmed-meshheading:19850104-Receptors, Complement
pubmed:year
2009
pubmed:articleTitle
Deletion of both the C3a and C5a receptors fails to protect against experimental autoimmune encephalomyelitis.
pubmed:affiliation
Department of Microbiology, University of Alabama at Birmingham, Birmingham, AL 35294, United States.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural