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• W2062464543 abstract "Dendritic cells (DCs) are central to the innate and adaptive responses needed to control pathogens, yet HIV exploits DCs to promote infection. The influence of other pathogens on DC-HIV interplay has not been extensively studied. We used Candida albicans (Candida) as a model pathogen which elicits innate DC responses that are likely important in controlling Candida by healthy immune systems. HIV did not impede Candida-specific DC activation. Candida-induced CD80 and CD83 upregulation was greater in DCs that had captured HIV, coinciding with increased amplification in presence of T cells and reduced but persistent low-level DC infection. In contrast, HIV-infected DCs matured normally in response to Candida, but this did not shut down HIV replication in DCs, and again Candida augmented HIV amplification in DC-T-cell mixtures. HIV-infected DCs secreted more IL-10 and IL-1β earlier than uninfected DCs and initially induced a higher frequency of CD4+CD25+FoxP3+ T-regulatory cells in response to Candida. Elevated early IL-10 production in cocultures was evident only when azidothymidine (AZT) was included to limit T-regulatory cell infection and destruction. Therefore, HIV manipulates the DC's innate and adaptive responses to Candida to further augment HIV spread, ultimately destroying the cells needed to limit candidiasis." @default.
• W2062464543 created "2016-06-24" @default.
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• W2062464543 date "2008-08-01" @default.
• W2062464543 modified "2023-10-16" @default.
• W2062464543 title "Candida albicans-Induced DC Activation Partially Restricts HIV Amplification in DCs and Increases DC to T-Cell Spread of HIV" @default.
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• W2062464543 doi "https://doi.org/10.1097/qai.0b013e3181776bc7" @default.
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