Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1996-6-27
pubmed:abstractText
Survival of acute Trypanosoma cruzi infection by mice is influenced by genes inside and outside the major histocompatibility complex (MHC) and genes associated with resistance must be expressed in both the MHC and the genetic background or the host will die within a few weeks of infection. Both the levels and the kinetics of cytokine production have also been implicated as important factors for resistance. Antigen-stimulated spleen cells from mice that express the resistant H-2q MHC haplotype produced significantly more interferon (IFN)-gamma than did cells from mice that share the susceptible H-2k haplotype. But, spleen cells from susceptible and resistant mice produce similar levels of IFN-gamma when stimulated with concanavalin A. The kinetics of interleukin (IL)- 10 production by ConA (ConA)-stimulated spleen cell were inversely correlated with IFN-gamma levels throughout the course of acute infection in all mouse strains. Levels of IL-2 produced by ConA-stimulated spleen cells were also initially high (day 0) then decreased as acute infection progressed. Conversely, IL-4 production by ConA-stimulated spleen cells increased during infection, and mice that express the susceptible C3H background produced significantly more IL-4 than those that share the resistant B10 background. IL-2 production by lymph node cells from mice that express the susceptible C3H genetic background also declined during infection, while lymph node cells from B10 background mice showed a moderate increase in IL-2 secretion. These data suggest that both the levels and the kinetics of cytokine production may be genetically regulated and that cytokine responses are compartmentalized in the T. cruzi-infected host.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0022-3395
pubmed:author
pubmed:issnType
Print
pubmed:volume
82
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
59-65
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:8627502-Animals, pubmed-meshheading:8627502-Cells, Cultured, pubmed-meshheading:8627502-Chagas Disease, pubmed-meshheading:8627502-Concanavalin A, pubmed-meshheading:8627502-Disease Susceptibility, pubmed-meshheading:8627502-Enzyme-Linked Immunosorbent Assay, pubmed-meshheading:8627502-Hybridomas, pubmed-meshheading:8627502-Immunity, Innate, pubmed-meshheading:8627502-Interferon-gamma, pubmed-meshheading:8627502-Interleukin-10, pubmed-meshheading:8627502-Interleukin-2, pubmed-meshheading:8627502-Interleukin-4, pubmed-meshheading:8627502-Interleukin-5, pubmed-meshheading:8627502-Interleukins, pubmed-meshheading:8627502-Kinetics, pubmed-meshheading:8627502-Lymph Nodes, pubmed-meshheading:8627502-Mice, pubmed-meshheading:8627502-Mice, Inbred C3H, pubmed-meshheading:8627502-Spleen
pubmed:year
1996
pubmed:articleTitle
Host genetics and resistance to acute Trypanosoma cruzi infection in mice: profiles and compartmentalization of IL-2-, -4-, -5-, -10-, and IFN-gamma-producing cells.
pubmed:affiliation
Department of Biological Sciences, Ohio University, Athens 45701, USA.
pubmed:publicationType
Journal Article