Candida albicans-induced DC activation partially restricts HIV amplification in DCs and increases DC to T-cell spread of HIV
| Autor: | Melissa Robbiani, Jeffrey D. Lifson, Vennansha G. Williams, Laurence Vachot, Julian W. Bess |
|---|---|
| Rok vydání: | 2008 |
| Předmět: |
T cell
Interleukin-1beta Immunoglobulins chemical and pharmacologic phenomena Cell Count HIV Infections T-Lymphocytes Regulatory Virus Immune system Antigen Antigens CD Candida albicans medicine Humans Pharmacology (medical) Membrane Glycoproteins biology Candidiasis virus diseases HIV Forkhead Transcription Factors Dendritic cell Dendritic Cells biology.organism_classification Virology Coculture Techniques Interleukin-10 Infectious Diseases medicine.anatomical_structure Lentivirus Immunology B7-1 Antigen CD80 |
| Zdroj: | Journal of acquired immune deficiency syndromes (1999). 48(4) |
| ISSN: | 1525-4135 |
| Popis: | 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-1beta earlier than uninfected DCs and initially induced a higher frequency of CD4CD25FoxP3 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. |
| Databáze: | OpenAIRE |
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