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Transcriptional regulation of HIV‐1 LTR during antigen‐dependent activation of primary T cells by dendritic cells
Author(s) -
TsunetsuguYokota Yasuko,
Kato Tamami,
Yasuda Sachiko,
Matsuda Zene,
Suzuki Yoichi,
Koyanagi Yoshio,
Yamamoto Naoki,
Akagawa Kiyoko,
Cho Michael W.,
Takemori Toshitada
Publication year - 2000
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.67.3.432
Subject(s) - biology , cd28 , t cell , hiv long terminal repeat , microbiology and biotechnology , antigen presenting cell , long terminal repeat , viral replication , antigen , dendritic cell , transcription factor , virus , virology , cd8 , immunology , gene expression , immune system , gene , genetics
Numerous factors are known to bind human immunodeficiency virus (HIV) long terminal repeat (LTR) and activate viral transcription, but little is known as to how they function in naturally activated T cells and to what extent their binding is relevant to HIV replication in vivo. To characterize the HIV LTR‐binding factors responsible for antigen‐dependent activation of HIV, we examined replication of LTR mutant viruses in CD4 + T cells activated by different stimuli. NF‐κB or Sp1 mutant virus replicated well in CD4 + T cells activated by phorbol ester and calcium ionophore. When they were activated by antigen‐pulsed dendritic cells, the replication of the Sp1‐deleted virus was severely impaired in CD45RA + , but not in CD45RO + T cell subsets that dominantly produce interleukin‐2 (IL‐2). Stimulation via CD3/CD28 induced a high level of IL‐2 production in both T cell subsets, but Sp1‐deleted virus poorly replicated in CD45RA + subset. The level of NF‐κB and Sp1‐binding factors did not differ between these subsets. Our results suggest that additional cofac‐tors distinct from IL‐2‐inducing signaling molecules are important for LTR activation during antigen‐dependent T cell activation. J. Leukoc. Biol. 67: 432–440; 2000.