Linked Life Data

9287187

Source:http://linkedlifedata.com/resource/pubmed/id/9287187

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1997-11-13
pubmed:abstractText
Virus infections cause a much more profound perturbation of the lymphoid tissue than can be accounted for by the exigencies of the antigen-specific response. The extent of this 'immunological dissonance' is seen most dramatically in mice infected with a persistent gamma-herpesvirus, MHV-68. A profile of massive, continuing proliferation of both T and B cells in the lymph nodes and spleen leads to a dramatic increase in the prevalence of a CD62Llow CD8+ T cell subset in the blood, a pattern first detected two to three weeks after intranasal exposure to the inducing virus. This syndrome, which seems identical to human infectious mononucleosis (IM), persists for a further month or more. Part of the IM-like phase of MHV-68 infection reflects the selective expansion of Vbeta4+ CD8+ T cells, with the Vbeta4 effect being apparent for several different MHC class I H-2 types but not in mice that are deficient in MHC class II glycoprotein expression. Depleting CD4(+) T helper cells in MHV-68-infected mice leads to the decreased proliferation of the CD8+ T cells in the spleen and fewer CD62Llow CD8+ T lymphocytes than would be expected in peripheral blood, but fails to diminish the prominence of the V4beta+ CD8+ population. The results so far of this unique experimental mouse model of IM suggest that both cytokine-mediated effects and a viral superantigen are operating to promote the dramatic expansion and persistence of activated CD8+ T cells in the vascular compartment.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0952-7915
pubmed:author
pubmed:issnType
Print
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
477-83
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:9287187-Animals, pubmed-meshheading:9287187-Antigens, Viral, pubmed-meshheading:9287187-CD4-Positive T-Lymphocytes, pubmed-meshheading:9287187-Cytokines, pubmed-meshheading:9287187-Disease Models, Animal, pubmed-meshheading:9287187-Gene Rearrangement, beta-Chain T-Cell Antigen Receptor, pubmed-meshheading:9287187-Herpesvirus 4, Human, pubmed-meshheading:9287187-Histocompatibility Antigens Class II, pubmed-meshheading:9287187-Humans, pubmed-meshheading:9287187-Infectious Mononucleosis, pubmed-meshheading:9287187-Lymphocyte Activation, pubmed-meshheading:9287187-Lymphocyte Cooperation, pubmed-meshheading:9287187-Lymphoid Tissue, pubmed-meshheading:9287187-Mice, pubmed-meshheading:9287187-Mice, Inbred C57BL, pubmed-meshheading:9287187-Receptors, Antigen, T-Cell, alpha-beta, pubmed-meshheading:9287187-Superantigens
pubmed:year
1997
pubmed:articleTitle
Tuning into immunological dissonance: an experimental model for infectious mononucleosis.
pubmed:affiliation
Department of lmmunology, St Jude Children's Research Hospital, 332 North Lauderdale, Memphis, TN 38105, USA. <peter.doherty@stjude.org
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't