期刊
JOURNAL OF VIROLOGY
卷 76, 期 22, 页码 11570-11583出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.76.22.11570-11583.2002
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资金
- NCI NIH HHS [CA64416] Funding Source: Medline
- NCRR NIH HHS [M01 RR000042, M01-RR00042] Funding Source: Medline
- NHLBI NIH HHS [HL63614, HL57885, HL39926, R01 HL063614] Funding Source: Medline
- NIAID NIH HHS [AI 07528, T32 AI007528, AI36685] Funding Source: Medline
- NIDCR NIH HHS [DE13161] Funding Source: Medline
- NIGMS NIH HHS [T32 GM007315, GM07315, T32 GM07863, T32 GM007863] Funding Source: Medline
The development of the complex neoplasm Kaposi's sarcoma is dependent on infection with the Kaposi's sarcoma-associated herpesvirus (KSRV) and appears to be greatly enhanced by cytokines and human immunodeficiency virus type 1 (HIV-1) Tat. Interleukin-8 (IL-8) and growth-regulated oncogene alpha (GRO-alpha) are chemokines involved in chemoattraction, neovascularization, and stimulation of HIV-1 replication. We have previously demonstrated that production of GRO-alpha is stimulated by exposure of monocyte-derived macrophages (MDM) to HIV-1. Here we show that exposure of MDM to HIV-1, viral Tat, or viral gp120 leads to a substantial increase in IL-8 production. We also demonstrate that IL-8 and GRO-alpha are induced by KSHV infection of endothelial cells and are crucial to the angiogenic phenotype developed by KSHV-infected endothelial cells in cell culture and upon implantation into SCID mice. Thus, the three known etiological factors in Kaposi's sarcoma pathogenesis-KSHV, HIV-1 Tat, and cellular growth factors-might be linked, in part, through induction of IL-8 and GRO-alpha.
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