rdf:type |
|
lifeskim:mentions |
umls-concept:C0021311,
umls-concept:C0021758,
umls-concept:C0038952,
umls-concept:C0041217,
umls-concept:C0085732,
umls-concept:C0242723,
umls-concept:C0439849,
umls-concept:C0445223,
umls-concept:C1552599,
umls-concept:C1704787,
umls-concept:C2587213
|
pubmed:issue |
8
|
pubmed:dateCreated |
1996-12-17
|
pubmed:databankReference |
|
pubmed:abstractText |
We studied non-MHC gene-dependent expression of a number of cytokines in relation to host defense and survival during Trypanosoma brucei brucei (Tbb) infection in mice. In particular, the role of IL-4 was explored with use of genomically IL-4-disrupted mice and in vivo Ab blocking. Splenocytes from MHC-identical B10.Q (relatively resistant) mice showed day 5 postinfection higher numbers of IL-4 mRNA expressing cells than C3H.Q (highly susceptible). A trypanosome-derived lymphocyte triggering factor, which is released by Tbb to polyclonally activate CD8+ T cells, stimulated naive splenocytes in vitro to a higher IL-4 response in B10.Q than in C3H.Q mice. The C3H.Q mice developed an extremely high parasitemia, showed a low Ab response against the variant surface glycoprotein (VSG), and had a mean survival time of 42 days. Conversely, B10.Q mice had lower parasitemia, mounted higher anti-VSG response, and had a mean survival time of 56 days. Deletion of the IL-4 gene had no influence on the infection in C3H.Q mice, while in B10.Q mice the deletion was associated with lower anti-VSG Ab levels and higher parasitemia. Paradoxically, B10.Q mice with disrupted IL-4 gene survived longer than the wild type. Anti-IL-4 Ab-blocking experiments in vivo displayed an enhanced parasitemia and prolonged survival in infected B10.Q mice. We conclude that 1) a non-MHC gene-related and CD8+-dependent ability to produce IL-4 partly determines the susceptibility to Tbb infection; and 2) IL-4, although involved in controlling the levels of parasitemia by its effects on immunoglobulin synthesis, also can have toxic effects on the animals.
|
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 |
157
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
3518-26
|
pubmed:dateRevised |
2006-11-15
|
pubmed:meshHeading |
pubmed-meshheading:8871651-Animals,
pubmed-meshheading:8871651-Antibodies, Blocking,
pubmed-meshheading:8871651-Antibodies, Protozoan,
pubmed-meshheading:8871651-Cytokines,
pubmed-meshheading:8871651-Female,
pubmed-meshheading:8871651-In Situ Hybridization,
pubmed-meshheading:8871651-Interleukin-4,
pubmed-meshheading:8871651-Male,
pubmed-meshheading:8871651-Mice,
pubmed-meshheading:8871651-Mice, Inbred C3H,
pubmed-meshheading:8871651-Mice, Inbred C57BL,
pubmed-meshheading:8871651-Mice, Knockout,
pubmed-meshheading:8871651-Molecular Sequence Data,
pubmed-meshheading:8871651-Parasitemia,
pubmed-meshheading:8871651-RNA, Messenger,
pubmed-meshheading:8871651-Species Specificity,
pubmed-meshheading:8871651-Trypanosoma brucei brucei,
pubmed-meshheading:8871651-Trypanosomiasis, African,
pubmed-meshheading:8871651-Variant Surface Glycoproteins, Trypanosoma
|
pubmed:year |
1996
|
pubmed:articleTitle |
Control of parasitemia and survival during Trypanosoma brucei brucei infection is related to strain-dependent ability to produce IL-4.
|
pubmed:affiliation |
Molecular Medicine Unit, Department of Medicine, Karolinska Hospital, Stockholm, Sweden. Moiz.Bakhiet@cnsf.ki.se
|
pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
|