Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions |
umls-concept:C0003241,
umls-concept:C0019185,
umls-concept:C0021311,
umls-concept:C0026809,
umls-concept:C0080194,
umls-concept:C0205225,
umls-concept:C0683598,
umls-concept:C0871261,
umls-concept:C1423842,
umls-concept:C1527148,
umls-concept:C1546857,
umls-concept:C1704632,
umls-concept:C1706817,
umls-concept:C2347662,
umls-concept:C2911692
|
| pubmed:issue |
9
|
| pubmed:dateCreated |
1996-6-13
|
| pubmed:abstractText |
Murine hepatitis virus strain 3 (MHV-3) produces a strain-dependent spectrum of disease. The development of liver necrosis has been shown to be related to production of a unique macrophage procoagulant activity (PCA), encoded by the gene fgl-2, in susceptible mice. These studies were designed to examine the influence of Th1/Th2 cells on resistance/susceptibility and production of macrophage PCA in resistant (A/J) and susceptible (BALB/cJ) strains of mice following infection with MHV-3. Immunization of A/J mice with MHV-3 induced a Th1 cellular immune response, and one Th1 cell line (3E9.1) protected susceptible mice and inhibited PCA production by macrophages both in vitro and in vivo. In contrast, immunization of BALB/cJ mice with an attenuated variant of MHV-3 derived from passaging MHV-3 in YAC-1 cells resulted in a Th2 response. Transfer of spleen cells and T cell lines from immunized BALB/cJ mice failed to protect naive susceptible syngeneic mice from infection with MHV-3 and augmented macrophage PCA production to MHV-3 in vitro. However, serum from immunized BALB/cJ mice contained high titrated neutralizing Ab that protected naive BALB/cJ animals from lethal primary MHV-3 infection. These results demonstrate that susceptible BALB/cJ mice generate a Th2 response following MHV-3 infection and that these Th2 cells neither inhibit MHV-3-induced macrophage PCA production nor protect naive mice from MHV-3 infection. The results suggest that Ab protects against primary infection but cannot eradicate ongoing infection. Thus, these data define the differential role of Th1/Th2 lymphocytes in primary and secondary MHV-3 infection and emphasize the importance of PCA in the pathogenesis of MHV-3 infection.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
May
|
| pubmed:issn |
0022-1767
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
1
|
| pubmed:volume |
156
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
3342-9
|
| pubmed:dateRevised |
2008-11-21
|
| pubmed:meshHeading |
pubmed-meshheading:8617959-Animals,
pubmed-meshheading:8617959-Antibodies, Viral,
pubmed-meshheading:8617959-Blood Coagulation Factors,
pubmed-meshheading:8617959-Cell Line,
pubmed-meshheading:8617959-Coronavirus Infections,
pubmed-meshheading:8617959-Disease Susceptibility,
pubmed-meshheading:8617959-Female,
pubmed-meshheading:8617959-Hepatitis, Viral, Animal,
pubmed-meshheading:8617959-Immunity, Innate,
pubmed-meshheading:8617959-Immunization, Passive,
pubmed-meshheading:8617959-Immunotherapy, Adoptive,
pubmed-meshheading:8617959-Macrophages,
pubmed-meshheading:8617959-Mice,
pubmed-meshheading:8617959-Mice, Inbred A,
pubmed-meshheading:8617959-Mice, Inbred BALB C,
pubmed-meshheading:8617959-Mice, Inbred C57BL,
pubmed-meshheading:8617959-Murine hepatitis virus,
pubmed-meshheading:8617959-Spleen,
pubmed-meshheading:8617959-Th1 Cells,
pubmed-meshheading:8617959-Th2 Cells,
pubmed-meshheading:8617959-Viral Vaccines
|
| pubmed:year |
1996
|
| pubmed:articleTitle |
Resistance of naive mice to murine hepatitis virus strain 3 requires development of a Th1, but not a Th2, response, whereas pre-existing antibody partially protects against primary infection.
|
| pubmed:affiliation |
Department of Surgery, The Toronto Hospital-University of Toronto, Ontario, Canada.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|