Human T-lymphotropic virus I-infected T cells constitutively express
lymphotoxin in vitro
E Tschachler, M Robert-Guroff, RC Gallo and MS Reitz
Laboratory of Tumor Cell Biology, National Cancer Institute, Bethesda, MD
20892.
We have studied the pattern of expression of the lymphokines tumor necrosis
factor (TNF alpha) and lymphotoxin (TNF beta) in T-cell lines established
by transformation with human T-lymphotropic virus, type I (HTLV-I), the
etiologic agent of adult T-cell leukemia (ATL). We report here that nine of
nine HTLV-I-infected T-cell lines, established by in vitro infection with
HTLV-I, including those with CD4+ or CD8+ as well as CD4-/CD8- phenotypes,
constitutively produce high levels of TNF alpha and -beta mRNA and secrete
biologically active TNF beta into the culture medium. Similar patterns of
expression are seen in six of six HTLV-I-infected T-cell lines directly
established from ATL patients. In contrast, several T-cell lines, either
uninfected or infected with human immunodeficiency virus I, did not produce
comparable levels of the TNF beta. Comparisons of a normal functional
T-cell clone before and after infection with HTLV-I show that expression of
TNF beta mRNA is induced in the infected cells. The high level expression
in HTLV-I- infected cell lines dose not seem to involve perturbation of the
TNF alpha/beta genetic loci by proviral integration. A cell line (81-66/45)
nonproductively transformed with HTLV-I that produces tat-1 in the absence
of viral structural proteins, produces both TNF alpha and -beta mRNA. This
suggests that expression of these cytokines could be mediated in trans by
the tat-1 gene product.
Volume 73,
Issue 1,
pp. 194-201,
01/01/1989
Copyright © 1989 by The American Society of Hematology
