Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
12
|
pubmed:dateCreated |
1996-1-18
|
pubmed:abstractText |
IL-2-deficient mice were used to examine the role of endogenous IL-2 for supporting T cell proliferative responses during infection with lymphocytic choriomeningitis virus (LCMV). The studies showed that, although virus-specific CTL activity was induced in the absence of IL-2, the overall magnitude of the response was profoundly inhibited. Examination of proportions and numbers of CD8+ T cells demonstrated that the normal virus-induced expansion of these cells was virtually eliminated in spleens and dramatically decreased in lymph nodes from IL-2-negative mice. Absence of endogenous IL-2 also significantly inhibited virus-induced activated T cell production of IFN-gamma, as well as increases in frequencies and numbers of IFN-gamma-producing cells. Reductions in immune responses were accompanied by impaired viral clearance. Although T cell responses were dramatically reduced in IL-2-deficient, as compared with IL-2-containing mice, activation signals were being delivered in vivo because induced CTLs were sensitive to the cell cycle-specific toxin, hydroxyurea (HU), and CD8+ T cells had induced expression of the IL-2R alpha- and beta-chains. These studies demonstrated that, although low levels of T cell responses can be induced in the absence of IL-2, the factor plays a unique and critical role in supporting T cell proliferative responses in vivo and in optimizing induction of the biologic functions mediated by these cells. Furthermore, the results identify a role for IL-2 in promoting IFN-gamma production in vivo.
|
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 |
15
|
pubmed:volume |
155
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
5690-9
|
pubmed:dateRevised |
2008-11-21
|
pubmed:meshHeading |
pubmed-meshheading:7499855-Animals,
pubmed-meshheading:7499855-Female,
pubmed-meshheading:7499855-Interferon-gamma,
pubmed-meshheading:7499855-Interleukin-2,
pubmed-meshheading:7499855-Lymphocyte Activation,
pubmed-meshheading:7499855-Lymphocytic Choriomeningitis,
pubmed-meshheading:7499855-Lymphocytic choriomeningitis virus,
pubmed-meshheading:7499855-Male,
pubmed-meshheading:7499855-Mice,
pubmed-meshheading:7499855-Mice, Mutant Strains,
pubmed-meshheading:7499855-Receptors, Interleukin-2,
pubmed-meshheading:7499855-T-Lymphocytes, Cytotoxic,
pubmed-meshheading:7499855-Virus Replication
|
pubmed:year |
1995
|
pubmed:articleTitle |
Endogenous IL-2 contributes to T cell expansion and IFN-gamma production during lymphocytic choriomeningitis virus infection.
|
pubmed:affiliation |
Division of Biology and Medicine, Brown University, Providence, RI 02912, USA.
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
|