Dendritic cells from the human female reproductive tract rapidly capture and respond to HIV
Autor: | Zheng Shen, Marta Rodriguez-Garcia, Christina Ochsenbauer, Margaret E. Ackerman, Austin W. Boesch, C.R. Wira, John C. Kappes, Fiona D. Barr |
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Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
Receptors CCR5 CD14 Immunology Lipopolysaccharide Receptors CD11c HIV Infections Receptors Cell Surface chemical and pharmacologic phenomena Biology DC-SIGN CD1c sex hormones Article antimicrobials CCL5 03 medical and health sciences 0302 clinical medicine Phagocytosis Humans Immunology and Allergy Macrophage Lectins C-Type Secretory Leukocyte Peptidase Inhibitor Cells Cultured Chemokine CCL2 Innate immunity Innate immune system Estradiol Interleukin-8 HIV Interleukin hemic and immune systems Dendritic Cells Genitalia Female Immunity Innate CD11c Antigen Elafin 3. Good health 030104 developmental biology CD103 Female Cell Adhesion Molecules 030215 immunology SLPI |
Zdroj: | Mucosal immunology |
ISSN: | 1933-0219 |
DOI: | 10.1038/mi.2016.72 |
Popis: | Dendritic cells (DCs) throughout the female reproductive tract (FRT) were examined for phenotype, HIV capture ability and innate anti-HIV responses. Two main CD11c+ DC subsets were identified: CD11b+ and CD11blow DCs. CD11b+CD14+ DCs were the most abundant throughout the tract. A majority of CD11c+CD14+ cells corresponded to CD1c+ myeloid DCs, whereas the rest lacked CD1c and CD163 expression (macrophage marker) and may represent monocyte-derived cells. In addition, we identified CD103+ DCs, located exclusively in the endometrium, whereas DC-SIGN+ DCs were broadly distributed throughout the FRT. Following exposure to GFP-labeled HIV particles, CD14+ DC-SIGN+ as well as CD14+ DC-SIGN− cells captured virus, with ∼30% of these cells representing CD1c+ myeloid DCs. CD103+ DCs lacked HIV capture ability. Exposure of FRT DCs to HIV induced secretion of CCL2, CCR5 ligands, interleukin (IL)-8, elafin, and secretory leukocyte peptidase inhibitor (SLPI) within 3 h of exposure, whereas classical pro-inflammatory molecules did not change and interferon-α2 and IL-10 were undetectable. Furthermore, elafin and SLPI upregulation, but not CCL5, were suppressed by estradiol pre-treatment. Our results suggest that specific DC subsets in the FRT have the potential for capture and dissemination of HIV, exert antiviral responses and likely contribute to the recruitment of HIV-target cells through the secretion of innate immune molecules. |
Databáze: | OpenAIRE |
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