Differential Level in Co-Down-Modulation of CD4 and CXCR4 Primed by HIV-1 gp120 in Response to Phorbol Ester, PMA, among HIV-1 Isolates

J-STAGE
  • Tahara-Hanaoka Satoko
    Department of Immunology, Institute of Basic Medical Sciences, University of Tsukuba
  • Ushijima Yuki
    Microbiological Genetics Division, Institute of Genetic Resources, Faculty of Agriculture, Kyushu University
  • Tarui Hiroshi
    Microbiological Genetics Division, Institute of Genetic Resources, Faculty of Agriculture, Kyushu University
  • Wada Masayuki
    Microbiological Genetics Division, Institute of Genetic Resources, Faculty of Agriculture, Kyushu University
  • Hara Toshio
    Microbiological Genetics Division, Institute of Genetic Resources, Faculty of Agriculture, Kyushu University
  • Imanishi Shigeo
    Laboratory of Cell Engineering, National Institute of Sericultural and Entomological Science
  • Yamaguchi Tomoyuki
    Department of Immunology, Institute of Basic Medical Sciences, University of Tsukuba
  • Hattori Toshio
    Division of Allergy and Infectious Diseases, Internal Medicine, Graduate School of Medicine, Tohoku University
  • Nakauchi Hiromitsu
    Department of Immunology, Institute of Basic Medical Sciences, University of Tsukuba
  • Koito Atsushi
    Division of Clinical Retrovirology and Infectious Diseases, Center for AIDS Research, Kumamoto University

抄録

HIV-1 enters cells through interacting with cell surface molecules such as CD4 and chemokine receptors. We generated recombinant soluble gp120s derived from T-cell line-tropic (T-tropic) and macrophage-tropic (M-tropic) HIV-1 strains using a baculovirus expression system and investigated the association of CD4-gp120 complex with the chemokine receptor and/or other surface molecule(s). For monitoring the co-down-modulations of the CD4-gp120 complex, a cytoplasmic domain deletion mutant (tailless CD4), which is not capable of undergoing down-modulation by itself in response to phorbol ester PMA, was used. Our studies revealed both cell-type and HIV-1 strain-specific differences. We found that T-tropic gp120s were capable of priming co-down-modulation with tailless CD4 by interacting with CXCR4, whereas M-tropic SF162 gp120 could not after PMA treatment even in the presence of CCR5. Among the T-tropic HIV-1 envelopes, IIIB gp120 was the most potent. Furthermore, the ability of gp120 to prime the PMA induced co-down-modulation of tailless CD4 appeared to be dependent on the concentration of the principal coreceptor CXCR4. Nevertheless, the observation that IIIB gp120 strongly primed tailless CD4 co-down-modulation on human osteosarcoma HOS cells that express undetectable levels of surface CXCR4 raised the possibility that membrane component(s) other than those recently identified can be involved in down-modulation of the CD4/gp120 complexes.

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