Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1983-2-25
pubmed:abstractText
The role of virulent forms of Trypanosoma cruzi in modulating mitogen-induced lymphocyte responses was investigated in this work. Bloodstream forms of T. cruzi inhibited normal mouse spleen cell responses to Con A and LPS in a dose-dependent manner. Reduced responses were observed over relatively large ranges of concentration of Con A (50-fold) and LPS (160-fold). The inhibitory action of the parasites could not be overcome by increasing the mitogen dose beyond optimal levels. Furthermore, absorption of mitogen solutions with four times as many parasites as used in the proliferation assays revealed that sufficient mitogen activity remained to produce optimal lymphocyte responses. Therefore, reduced lymphocyte responsiveness was not due to absorption of mitogen by the parasite. Inhibited responses were also seen when a sonicated T. cruzi preparation was used, indicating that parasite viability was not required to produce suppression. Inhibition of Con A- or LPS-induced responses by the parasites occurred only when the trypanosomes were incorporated into the system during the first 24 hr of culture. These results show that virulent forms of T. cruzi can induce suppression of T and B cell responses in vitro, and suggest that the parasite affects lymphocyte commitment to blastogenesis during the early stages of lymphocyte activation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:volume
130
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
908-11
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1983
pubmed:articleTitle
Inhibition of mitogen-induced proliferation of mouse T and B lymphocytes by bloodstream forms of Trypanosoma cruzi.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.