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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
|
| pubmed:dateCreated |
1992-9-14
|
| pubmed:abstractText |
The role and interdependence of CD8+ and CD4+ alpha beta-T cells in the acute response after respiratory infection with the murine parainfluenza type 1 virus, Sendai virus, has been analyzed for H-2b mice. Enrichment of CD8+ virus-specific CTL effectors in the lungs of immunologically intact C57BL/6 animals coincided with the clearance of the virus from this site by day 10 after infection. Removal of the CD4+ T cells by in vivo mAb treatment did not affect appreciably either the recruitment of CD8+ T cells to the infected lung, or their development into virus-specific cytotoxic effectors. In contrast, depletion of the CD8+ subset delayed virus clearance, although most mice survived the infection. Transgenic H-2b F3 mice homozygous (-/-) for a beta 2 microglobulin (beta 2-m) gene disruption, which lack both class I MHC glycoproteins and mature CD8+ alpha beta-T cells, showed a comparable, delayed clearance of Sendai virus from the lung. Virus-specific, class II MHC-restricted CTL were demonstrated in both freshly isolated bronchoalveolar lavage populations and cultured lymph node and spleen tissue from the beta 2-m (-/-) transgenics. Treatment of the beta 2-m (-/-) mice with the mAb to CD4 led to delayed virus clearance and death, which was also the case for normal mice that were depleted simultaneously of the CD4+ and CD8+ subsets. These results indicate that, although classical class I MHC-restricted CD8+ cytotoxic T cells normally play a dominant role in the recovery of mice acutely infected with Sendai virus, alternative mechanisms involving CD4+ T cells exist and can compensate, in time, for the loss of CD8+ T cell function.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Aug
|
| pubmed:issn |
0022-1767
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
15
|
| pubmed:volume |
149
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
1319-25
|
| pubmed:dateRevised |
2007-11-14
|
| pubmed:meshHeading |
pubmed-meshheading:1354233-Animals,
pubmed-meshheading:1354233-Antigens, CD8,
pubmed-meshheading:1354233-Bronchoalveolar Lavage Fluid,
pubmed-meshheading:1354233-CD4-Positive T-Lymphocytes,
pubmed-meshheading:1354233-Female,
pubmed-meshheading:1354233-Histocompatibility Antigens Class I,
pubmed-meshheading:1354233-Immunity, Cellular,
pubmed-meshheading:1354233-Lung,
pubmed-meshheading:1354233-Lymph Nodes,
pubmed-meshheading:1354233-Lymphocyte Depletion,
pubmed-meshheading:1354233-Major Histocompatibility Complex,
pubmed-meshheading:1354233-Mice,
pubmed-meshheading:1354233-Mice, Inbred Strains,
pubmed-meshheading:1354233-Mice, Transgenic,
pubmed-meshheading:1354233-Parainfluenza Virus 1, Human,
pubmed-meshheading:1354233-Paramyxoviridae Infections,
pubmed-meshheading:1354233-T-Lymphocyte Subsets,
pubmed-meshheading:1354233-T-Lymphocytes, Cytotoxic,
pubmed-meshheading:1354233-Virus Replication
|
| pubmed:year |
1992
|
| pubmed:articleTitle |
Delayed clearance of Sendai virus in mice lacking class I MHC-restricted CD8+ T cells.
|
| pubmed:affiliation |
Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|