期刊
JOURNAL OF IMMUNOLOGY
卷 180, 期 4, 页码 2029-2033出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.180.4.2029
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资金
- NCRR NIH HHS [RR 00166] Funding Source: Medline
- NIAID NIH HHS [AI 52203, AI 53146, AI 51386, AI 44257] Funding Source: Medline
- NIAMS NIH HHS [AR 7108] Funding Source: Medline
Use of the progesterone (Pg) birth control depot medroxyprogesterone acetate (DMPA) increases a woman's risk for sexually transmitted infection with HIV or HSV-2 via unknown mechanisms. Plasmacytoid dendritic cells (pDCs) are circulating and tissue-resident sentinels capable of making large quantities of IFN-alpha upon recognizing viruses through TLRs 7 and 9. In this study, we show that Pg inhibits TLR9-induced IFN-alpha production by human and mouse pDCs and that DMPA impairs TLR9- and virus-induced IFN-alpha production by pDCs in mice, providing a potential explanation for how DMPA impairs innate antiviral immunity in women. Pg failed to inhibit the Mda-5 pathway of IFN-alpha induction in dendritic cells, suggesting that Pg regulates select antiviral DC programs. This may occur through selective blockade of IFN regulatory factor-7 activation, a novel steroid action. Thus, through inhibition of M-mediated IFN-alpha production by pDCs, Pg may regulate antiviral immunity.
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