Linked Life Data

2251909

Source:http://linkedlifedata.com/resource/pubmed/id/2251909

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1991-1-17
pubmed:abstractText
To clarify the implication of the major histocompatibility complex class II (Ia) antigen induction in microglia following Wallerian degeneration in the central nervous system (CNS), experimental allergic encephalitis (EAE) was adoptively transferred to Lewis rats in which Ia antigens had been induced in microglia at the sites of Wallerian degeneration. In addition to randomly distributed typical EAE lesions, the recipient rats developed distinct inflammatory lesions in accord with the distribution of Ia-positive microglia; i.e., in the ipsilateral thalamus after cortical cryoinjury, and in the ipsilateral optic nerve, the contralateral optic tract and superior colliculus after unilateral eye ball enucleation. Thus, the EAE locus may be targeted by this approach. The inflammatory response was inducible by transfer of myelin basic protein-stimulated lymphocytes but not by transfer of phytohemagglutinin-stimulated or non-stimulated lymphocytes. When examined using monoclonal antibody surface markers; OX-6 for Ia antigen, W3/13 for pan T lymphocyte and OX-8 for cytotoxic/suppresser T lymphocyte, the types of lymphocytes in these lesions did not differ from those in ordinary EAE lesions in the spinal cord. The potential role of non-immunologically induced Ia-positive cell clusters that serve as a target for autoimmune CNS diseases was discussed.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0001-6322
pubmed:author
pubmed:issnType
Print
pubmed:volume
80
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
521-6
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Targeting of adoptively transferred experimental allergic encephalitis lesion at the sites of wallerian degeneration.
pubmed:affiliation
Department of Neurological Sciences, Tohoku University School of Medicine, Sendai, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't