Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1988-5-18
pubmed:abstractText
To explain previous findings that rodent and African trypanosomes are relatively insusceptible to the actions of NK cells, their sensitivity to the cytotoxicity of rat LGL tumor cells and isolated cytolysin-containing granules was studied. LGL tumor cells displayed modest spontaneous killing of rodent trypanosomes but were considerably more effective in the antibody-dependent cell-mediated cytotoxicity mode in the presence of specific antibody. The trypanosomes were quite resistant to lysis by the cytolysin-containing granules, compared with other types of cells. The slow inefficient lysis that occurred in the presence of divalent cations involved granule concentrations thousands of times greater than was required for lysis of SRBC. Rodent trypanosomes were significantly more susceptible to lysis when divested of their surface glycoprotein coats. In the absence (or near absence) of divalent cations, a substance (or substances) present in the granules rapidly destroyed intact and nude trypanosomes; this activity probably was not associated with cytolysin. The rate and efficiency with which the divalent cation-independent substance destroyed three species of trypanosomes indicate that this material deserves further study with an eye to its potential use as a therapeutic agent.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
140
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2774-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
The toxicity of rat large granular lymphocyte tumor cells and their cytoplasmic granules for rodent and African trypanosomes.
pubmed:affiliation
Department of Microbiology, George Washington University School of Medicine, Washington, DC 20037.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.