Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1996-11-1
pubmed:abstractText
Regulation of experimental autoimmune encephalomyelitis (EAE) in Lewis rats may involve activation-dependent negative feedback pathways of T-helper cells. Previous studies have shown that T-helper cells specific for myelin basic protein exhibit a postactivation refractory phase during which antigenic restimulation elicits proliferation without production of IL-2. Herein, we show that postactivation refractoriness inhibits regeneration of EAE transfer activity and is manifest by a lack of IL-2 mRNA accumulation despite induction of normal levels of IL-4 mRNA. Preactivated refractory T cells were substantially more susceptible than resting T cells to the induction of anergy. Low-density T cell activation or subcloning prolonged the duration of the refractory phase and engendered long-term desensitization of T cells marked by a blockade of IL-2 production and by enhanced susceptibility to anergy. Overall, these results support the concept that postactivation refractoriness controls the pathogenicity and differentiation of T-helper cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0008-8749
pubmed:author
pubmed:issnType
Print
pubmed:day
25
pubmed:volume
172
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
108-17
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
T-helper lymphocytes specific for myelin basic protein: low-density activation prolongs a postactivation refractory phase marked by decreased pathogenicity and enhanced sensitivity to anergy.
pubmed:affiliation
Department of Microbiology and Immunology, East Carolina University School of Medicine, North Carolina, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't