Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
|
| pubmed:dateCreated |
1996-12-12
|
| pubmed:abstractText |
Control of the acute phase of Trypanosoma cruzi infections is critically dependent on cytokine-mediated macrophage activation to intracellular killing. We investigated the roles of IL-10, TNF, IFN-gamma, and IL-12 in the control of parasitism by innate and specific immunity. Mice with disrupted IL-10 genes (IL-10 KO) infected with Y strain T. cruzi have lower parasite numbers in the blood and tissues and higher IFN-gamma and nitric oxide (NO) production by spleen cells than wild type (WT) mice. Treatment of IL-10 KO and WT mice with recombinant IL-10 resulted in increased parasitemia. Mice with disrupted recombinase-activating genes (RAG/KO) that lack B and T cells provided a model for determining the importance of innate immunity to resistance. RAG/KO and WT mice had similar parasitemia levels until Day 13 of infection, suggestive of effective control of parasitism by the innate immune system during the early phase of infection; from them on parasitemia was higher in RAG/KO. Double RAG/IL-10 KO mice and RAG/KO mice had superimposable parasitemia curves, indicating that in the absence of T and B cells, endogenous IL-10 does not limit the efficacy of the innate immune system. Treatment of infected RAG/KO, IL-10/KO, and WT mice with anti-IFN-gamma, anti-TNF, or anti-IL-12 neutralizing mAbs increased parasitemia levels showing the importance of endogenous production of these cytokines in the control of parasitism by innate and specific immune responses. Spleen cells from anti-IL 12-treated WT mice had diminished production of IFN-gamma and NO, suggesting that early IFN-gamma synthesis is most dependent on IL-12 stimulation.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-10,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-12,
http://linkedlifedata.com/resource/pubmed/chemical/Nitrites,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Nov
|
| pubmed:issn |
0014-4894
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
84
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
231-44
|
| pubmed:dateRevised |
2008-11-21
|
| pubmed:meshHeading |
pubmed-meshheading:8932773-Animals,
pubmed-meshheading:8932773-Antibodies, Monoclonal,
pubmed-meshheading:8932773-Cells, Cultured,
pubmed-meshheading:8932773-Chagas Disease,
pubmed-meshheading:8932773-Dendritic Cells,
pubmed-meshheading:8932773-Female,
pubmed-meshheading:8932773-Immunity, Active,
pubmed-meshheading:8932773-Immunity, Innate,
pubmed-meshheading:8932773-Interferon-gamma,
pubmed-meshheading:8932773-Interleukin-10,
pubmed-meshheading:8932773-Interleukin-12,
pubmed-meshheading:8932773-Keratinocytes,
pubmed-meshheading:8932773-Lymphocytes,
pubmed-meshheading:8932773-Macrophages,
pubmed-meshheading:8932773-Male,
pubmed-meshheading:8932773-Mice,
pubmed-meshheading:8932773-Nitrites,
pubmed-meshheading:8932773-Parasitemia,
pubmed-meshheading:8932773-Spleen,
pubmed-meshheading:8932773-Trypanosoma cruzi,
pubmed-meshheading:8932773-Tumor Necrosis Factor-alpha
|
| pubmed:year |
1996
|
| pubmed:articleTitle |
Trypanosoma cruzi: IL-10, TNF, IFN-gamma, and IL-12 regulate innate and acquired immunity to infection.
|
| pubmed:affiliation |
Departamento de Imunologia, Universidade de Säo Paulo, Brasil.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|