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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1976-3-18
pubmed:abstractText
Blood lymphocytes from twenty-three untreated patients with Hodgkin's disease and twelve healthy controls were studied for their ability to lyse tissue culture cells (Chang cells) labelled with [51Cr]chromate. Lysis induced by patients' lymphocytes in the presence of PHA or rabbit IgG antibodies to Chang cells (ACS) was impaired in some, and higher than normal in others. ACS-induced lysis showed some corlation with the content of lymphocytes carrying receptors for human complement (CRL) in the effectory population. No correlation with immunoglobulin-bearing cells was noted. PHA-induced cytoxicity did not correlate with lymphocyte subpopulations. The observations are consistent with the assumption that effector cells of antibody-induced lymphocyte-mediated cytotoxicity (K cells) may be present among CRL. The K-cell activity and PHA cytotoxicity by lymphocytes tended to decrease at high age, but impaired cytotoxity was also noted in young patients. A preliminary follow-up of patients 1-2 years after the beginning of treatment revealed almost abolished K-cell activity in four patients who died 6--13 months after testing. Patients in incomplete remission or with relapse after treatment had lower mean K-cell activity than those in complete remission. A similar, but less pronounced tendency was found for PHA-induced cytotoxicity. A prognostic role of impaired K-cell activity in Hodgkin's disease is suggested from these data, but requires confirmation in a larger clinical follow-up.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0009-9104
pubmed:author
pubmed:issnType
Print
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
376-83
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1975
pubmed:articleTitle
Cytotoxic activity of lymphocytes from patients with Hodgkin's disease.
pubmed:publicationType
Journal Article