Linked Life Data

12471147

Source:http://linkedlifedata.com/resource/pubmed/id/12471147

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2002-12-9
pubmed:abstractText
Experimental autoimmune encephalomyelitis (EAE) serves as a model for multiple sclerosis and is considered a CD4(+), Th1 cell-mediated autoimmune disease. IL-12 is a heterodimeric cytokine, composed of a p40 and a p35 subunit, which is thought to play an important role in the development of Th1 cells and can exacerbate EAE. We induced EAE with myelin oligodendrocyte glycoprotein (MOG) peptide 35-55 (MOG(35-55)) in C57BL/6 mice and found that while IL-12p40-deficient (-/-) mice are resistant to EAE, IL-12p35(-/-) mice are susceptible. Typical spinal cord mononuclear cell infiltration and demyelination were observed in wild-type and IL-12p35(-/-) mice, whereas IL-12p40(-/-) mice had normal spinal cords. A Th1-type response to MOG(35-55) was observed in the draining lymph node and the spleen of wild-type mice. A weaker MOG(35-55)-specific Th1 response was observed in IL-12p35(-/-) mice, with lower production of IFN-gamma. By contrast, a Th2-type response to MOG(35-55) correlated with disease resistance in IL-12p40(-/-) mice. Production of TNF-alpha by microglia, CNS-infiltrating macrophages, and CD4(+) T cells was detected in wild-type and IL-12p35(-/-), but not in IL-12p40(-/-), mice. In addition, NO production was higher in IL-12p35(-/-) and wild-type mice than in IL-12p40(-/-) mice. These data demonstrate a redundancy of the IL-12 system in the induction of EAE and suggest that p40-related heterodimers, such as the recently cloned IL-23 (p40p19), may play an important role in disease pathogenesis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
169
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
7104-10
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:12471147-Animals, pubmed-meshheading:12471147-Cytokines, pubmed-meshheading:12471147-Demyelinating Autoimmune Diseases, CNS, pubmed-meshheading:12471147-Encephalomyelitis, Autoimmune, Experimental, pubmed-meshheading:12471147-Female, pubmed-meshheading:12471147-Genetic Predisposition to Disease, pubmed-meshheading:12471147-Glycoproteins, pubmed-meshheading:12471147-Immunity, Innate, pubmed-meshheading:12471147-Immunodominant Epitopes, pubmed-meshheading:12471147-Injections, Subcutaneous, pubmed-meshheading:12471147-Interleukin-12, pubmed-meshheading:12471147-Interleukin-12 Subunit p35, pubmed-meshheading:12471147-Interleukin-12 Subunit p40, pubmed-meshheading:12471147-Mice, pubmed-meshheading:12471147-Mice, Inbred C57BL, pubmed-meshheading:12471147-Mice, Knockout, pubmed-meshheading:12471147-Nitric Oxide, pubmed-meshheading:12471147-Peptide Fragments, pubmed-meshheading:12471147-Protein Subunits, pubmed-meshheading:12471147-Spinal Cord, pubmed-meshheading:12471147-Tumor Necrosis Factor-alpha
pubmed:year
2002
pubmed:articleTitle
IL-12p35-deficient mice are susceptible to experimental autoimmune encephalomyelitis: evidence for redundancy in the IL-12 system in the induction of central nervous system autoimmune demyelination.
pubmed:affiliation
Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't