Linked Life Data

2459230

Source:http://linkedlifedata.com/resource/pubmed/id/2459230

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1988-11-9
pubmed:abstractText
The relative contributions of IL-2 and IL-4 during the immune response to the retrovirus-induced tumor, FBL, were examined. Both proliferative and cytolytic responses to FBL were measured and compared to similar responses to minor histocompatibility Ag. The addition of alpha IL-2 partially inhibited FBL-stimulated proliferation of purified L3T4+ T cells and nearly completely inhibited the response of Lyt-2+ T cells, whereas alpha IL-4 partially inhibited the proliferative response of the L3T4+ subset but had no effect on the response of the Lyt-2+ subset. The addition of exogenous IL-4 augmented the proliferative response of both subsets. Therefore, IL-4 is an endogenous growth factor for FBL-induced specific proliferation of the L3T4+ and not the Lyt-2+ population, but both subpopulations can respond to IL-4. Similar examination of anti-FBL CTL responses revealed that alpha IL-2, but not alpha IL-4, inhibited FBL-specific Lyt-2+ CTL generation. However, exogenous IL-4 partially replaced the L3T4+ Th cell activity necessary for optimal Lyt-2+ FBL-specific CTL generation. Therefore, IL-4 is not required but can participate in the CTL response. The role of IL-4 during the immune response of B6 mice to minor histocompatibility Ag disparate BALB.B cells was analyzed. alpha IL-4 had no detectable effect on the proliferative or cytolytic response to BALB.B cells, suggesting that endogenous IL-4 does not have a significant role in these responses. The extent of involvement of endogenous IL-4 in the T cell responses to retrovirus-induced tumor Ag and minor histocompatibility Ag presumably reflects the nature of the stimulating Ag, and detection of an IL-4 response may correlate with induction of an antibody response. Thus, the immunizing Ag and/or host B cell repetoire may influence which subsets of L3T4+ Th cells are activated during priming in vivo.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
141
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2824-30
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:2459230-Animals, pubmed-meshheading:2459230-Antibodies, pubmed-meshheading:2459230-Antigens, Differentiation, T-Lymphocyte, pubmed-meshheading:2459230-Cell Transformation, Viral, pubmed-meshheading:2459230-Epitopes, pubmed-meshheading:2459230-Female, pubmed-meshheading:2459230-Friend murine leukemia virus, pubmed-meshheading:2459230-Immunosuppressive Agents, pubmed-meshheading:2459230-Interleukin-2, pubmed-meshheading:2459230-Interleukin-4, pubmed-meshheading:2459230-Interleukins, pubmed-meshheading:2459230-Leukemia, Erythroblastic, Acute, pubmed-meshheading:2459230-Lymphocyte Activation, pubmed-meshheading:2459230-Mice, pubmed-meshheading:2459230-Mice, Inbred BALB C, pubmed-meshheading:2459230-Mice, Inbred C57BL, pubmed-meshheading:2459230-Mice, Inbred CBA, pubmed-meshheading:2459230-Spleen, pubmed-meshheading:2459230-T-Lymphocytes, Cytotoxic
pubmed:year
1988
pubmed:articleTitle
Il-4 is an endogenous T cell growth factor during the immune response to a syngeneic retrovirus-induced tumor.
pubmed:affiliation
Department of Microbiology/Immunology, University of Washington, Seattle 98195.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't