Was induction of HIV-1 through TLR9?
نویسندگان
چکیده
منابع مشابه
Impact of in vitro costimulation with TLR2, TLR4 and TLR9 agonists and HIV-1 on antigen-presenting cell activation.
OBJECTIVE HIV-1 infects several immune cells including dendritic cells (DCs) and monocytes, which contributes in both to dissemination of HIV-1 infection and induction of antiviral immunity. These cells produce high amounts of type I IFN and proinflammatory cytokines upon Toll-like receptor (TLR) stimulation. During HIV-1 infection, an altered production of proinflammatory cytokines has been re...
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Background: In the past decade, childlessness has become a most important problem in the world. At the same time evidence confirms a link between sexually transmitted diseases (STDs) and infertility problem. Some of viral STDs are: HIV, HPV, HSVand so on. The innate immune system is essential for the initial detection of invading viruses and subsequent activation of adaptive immunity. also, The...
متن کاملHIV-1 gp120 inhibits TLR9-mediated activation and IFN-{alpha} secretion in plasmacytoid dendritic cells.
Plasmacytoid dendritic cells (pDCs) play a central role in innate and adaptive immune responses against viral infections. pDCs secrete type I IFNs and proinflammatory cytokines upon stimulation by either TLR7 or TLR9. Throughout the course of HIV infection, the production of type-I IFNs is profoundly impaired, and total pDC cell counts in peripheral blood correlates inversely with viral load an...
متن کاملHIV-1 gp120 inhibits TLR9-mediated activation and IFN- secretion in plasmacytoid dendritic cells
Plasmacytoid dendritic cells (pDCs) play a central role in innate and adaptive immune responses against viral infections. pDCs secrete type I IFNs and proinflammatory cytokines upon stimulation by either TLR7 or TLR9. Throughout the course of HIV infection, the production of type-I IFNs is profoundly impaired, and total pDC cell counts in peripheral blood correlates inversely with viral load an...
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عنوان ژورنال:
- Journal of immunology
دوره 171 4 شماره
صفحات -
تاریخ انتشار 2003