Linked Life Data

9526842

Source:http://linkedlifedata.com/resource/pubmed/id/9526842

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1998-4-9
pubmed:abstractText
EAE is a Th1 cell-mediated inflammatory autoimmune demyelinating disease of the central nervous system. IL-12 is a 70 kd heterodimeric cytokine, capable of regulating a wide range of immune functions. In view of its crucial role in the development of Th1 immune responses, we studied the expression of IL-12 p40 in the CNS and lymphoid organs of mice with EAE. RT-PCR analysis showed an increase in the expression of IL-12 p40 in brain and spinal cord during the acute paralytic phase of EAE and that decreased upon clinical recovery. The expression of p40 mRNA was also increased in spleen, lymph node and liver along with an elevated levels of circulating serum IL-12 during the height of disease. In vivo administration of rIL-12 increased the proliferative response and IFN-gamma production of MBP sensitized T cells and that was decreased following treatment with anti-IL-12 antibody. The expression of IL-12 in the target and lymphoid organs of animals with EAE, the induction of a Th1 type immune response following immunization with neuronal antigens and the inhibition of clinical disease upon treatment with anti-IL-12 antibody, suggest the crucial role of IL-12 in the pathogenesis of EAE.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0165-5728
pubmed:author
pubmed:issnType
Print
pubmed:volume
82
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
22-30
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Expression of IL-12 in CNS and lymphoid organs of mice with experimental allergic encephalitis.
pubmed:affiliation
Multiple Sclerosis Research Laboratory, Vanderbilt Stallworth Rehabilitation Hospital, Nashville, TN 37212, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't