Linked Life Data

2147195

Source:http://linkedlifedata.com/resource/pubmed/id/2147195

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
1991-1-7
pubmed:abstractText
Cell-mediated immunity to Listeria monocytogenes (LM) involves both CD4+ and CD8+ T cell responses. An important virulence factor in the pathogenesis of infection and development of protective immunity to LM is secretion of the sulfhydryl-activated hemolysin (Hly), listeriolysin. Listeria secretion of Hly allows LM to escape the endosomal compartment and enter the cytosol of the cell where intracellular growth can occur. We developed a system using bone marrow macrophages cultured in CSF-1 or IFN-gamma for comparing the response of CD4+ or CD8+ T cells to heat-killed, live Hly-, and live Hly+ LM. Macrophages grown in CSF were permissive for intracellular growth of Hly+ but not Hly- LM. CD8+ T cells recognized Hly+ LM but not HK or Hly- LM pulsed macrophages. However, CD4+ T cells recognized all three Listeria preparations fed to IFN-gamma-treated macrophages. These results suggest that both heat-killed LM and live LM efficiently enter the exogenous pathway for class II Ag processing and presentation. In contrast, only Hly+ LM activates the class I pathway, probably as a result of Hly+ bacterial replication within the cytosolic compartment.
pubmed:grant
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
1
pubmed:volume
145
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3540-6
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Presentation of Listeria monocytogenes to CD8+ T cells requires secretion of hemolysin and intracellular bacterial growth.
pubmed:affiliation
Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.