PubMed:7530239 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PubMed/sourceid/7530239","sourcedb":"PubMed","sourceid":"7530239","source_url":"http://www.ncbi.nlm.nih.gov/pubmed/7530239","text":"Induction of ICAM-1 and LFA-3 by Tax1 of human T-cell leukemia virus type 1 and mechanism of down-regulation of ICAM-1 or LFA-1 in adult-T-cell-leukemia cell lines.\nThe present study was undertaken to determine the role of HTLV-I TaxI in the up-regulation of ICAM-I and LFA-3 in human T cells transformed with HTLV-I and the mechanism of down-regulation of ICAM-I and LFA-I in ATL-derived cell lines. Induction of TaxI in a human T-cell line Jurkat carrying the TaxI gene under the metallothionein promoter led to increases in mRNA and surface expression of ICAM-I. The response of LFA-3 to TaxI induction was, on the other hand, relatively slow and weak, and might be indirect. Transactivation of the ICAM-I promoter by TaxI was further shown by co-transfection of a CAT reporter construct with the ICAM-I promoter and a plasmid expressing TaxI. The mechanism of down-regulation of ICAM-I or LFA-I in 4 ATL cell lines was next examined. ICAM-I mRNA was quite low in MT-I, but no genomic changes were found. The CAT reporter with the ICAM-I promoter was inactive in MT-I. Finally, combined treatment of MT-I with 5-azacytidine and IFN-gamma induced re-expression of ICAM-I. Collectively, (a) transcriptional factor(s) necessary for expression of ICAM-I gene may be repressed in MT-I through DNA methylation. Three other ATL cell lines (TL-OmI, H582, HuT102) were found to have little mRNA for the LFA-I beta chain (CD18). H582 and HuT102 were also negative for the LFA-I alpha chain (CDIIa) mRNA. 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