Cd. Morgan et al., Induction of surface antigen CD69 expression in T-lymphocytes following exposure to actinomycin D, INT J IMMUN, 21(10), 1999, pp. 689-703
The expression of surface antigen CD69 in immune response cells is typicall
y associated with the early stage(s) of cell activation, with maximal expre
ssion levels within 4 h of appropriate antigenic or mitogenic stimulation,
and maintenance of these high expression levels for 18-24 h. The expression
profiles of CD69 in human peripheral blood mononuclear cells (PBMC)culture
d with actinomycin D prior to mitogenic stimulation were evaluated by direc
t immunofluorescence using flow cytometry. Pretreatment of PBMC suspensions
with low, non-toxic levels of actinomycin D stimulated CD3(+) T-lymphocyte
s to express CD69 in a concentration-dependent manner. Furthermore, CD4(+)
T-lymphocytes were the primary cells responding in this fashion. Secondary
mitogenic stimulation following antibiotic treatment potentiated cellular C
D69 expression in these assays. CD69 expression was profoundly suppressed w
ith in vitro actinomycin D concentrations greater than or equal to 1-2 mu g
/ml, presumably by interference with cellular transcription/translation mec
hanisms. Parallel thymidine incorporation assays indicated that actinomycin
D effectively inhibited thymidine uptake in a concentration-dependent mann
er, with complete inhibition at greater than or equal to 0.1 mu g/ml. The e
valuation of cell cycling dynamics following antibiotic treatment, with and
without secondary mitogen stimulation, indicated no substantial changes in
DNA synthesis over controls. The diversity of these responses suggests tha
t expression of CD69 may not solely reflect mitogenic activation status but
may, under some conditions, result from induced cellular stress. (C) 1999
International Society for Immunopharmacology. Published by Elsevier Science
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