2001 Fiscal Year Final Research Report Summary
Basic Research for AIDS control A02 ; Pathophysiology and immunology of HIV-1 infection
| Project/Area Number |
10180102
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| Research Category |
Grant-in-Aid for Scientific Research on Priority Areas (A)
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| Allocation Type | Single-year Grants |
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| Review Section |
Biological Sciences
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
UCHIYAMA Takashi Kyoto University, Graduate School of Medicine, Professor, 医学研究科, 教授 (80151900)
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| Co-Investigator(Kenkyū-buntansha) |
TAKAHASHI Hidemi Nippon Medical School, Professor, 医学部, 教授 (40221361)
KIYONO Hiroshi Osaka University, Research Institute for Microbial Diseases, Professor, 微生物病研究所, 教授 (10271032)
NAGASAWA Takashi Kyoto University, Institute for Frontier Medical Sciences, Professor, 再生医学研究所, 教授 (80281690)
YOSHIE Osamu Kinki University School of Medicine, Professor, 医学部, 教授 (10166910)
TAKIGUCHI Masafumi Kumamoto University, Center for AIDS Research, Professor, エイズ学研究センター, 教授 (00183450)
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| Project Period (FY) |
1998 – 2001
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| Keywords | HIV-1 / AIDS / Pathophysiology / Immune response / AIDS Control / Chemokine / Chemokine Receptor / dendritic cells |
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| Research Abstract |
We have been worked mainly on chemokine/chemokine receptor system in HIV-1 infection and HIV-1-specific CTL, and got many results as described below. Uchiyama reported that natural alpha interferon-producing cells, which was a precursor of certain dendritic cell subsets and played a crucial role in an innate immune response, could be infected with HIV-1 and produce a large amount of alpha interferon in response to HIV-1 infection to differentiate into dendritic cells. Nagasawa identified a subset of the most immature precursor B cells and showed that SDF-1 is essential for the development of this cell subset using various knockout mice. Yoshie analyzed the role of immune chemokine constitutively expressed in lymphoid organs in HIV-1 infection. He also analyzed the suppressive effect of P2G-SDF-1-Fc chimeric protein on HIV-1 infection. Kiyono reported that immunization with gp160-fusogenic liposome through nasal mucosa induced the neutralizing antibodies response in not only wild type mice but also IFN-γ-knockout mice or IL-4-knockout mice, indicating a possible implication of this vaccine as a therapeutic vaccine. Takahashi reported detailed mechanism of CTL response to HIV-1 infection. Takizawa found that HIV-1-specific CD8(+) CTL expressed CCR5 on their surfaces and migrated by this ligand, indicating that these chemikines might be involved in the induction of Th1 response.
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