Human type 2 myeloid dendritic cells produce interferon-λ and amplify interferon-α in response to hepatitis C virus infection.
Human type 2 myeloid dendritic cells produce interferon-λ and amplify interferon-α in response to hepatitis C virus infection.
复制标题
人类 2 型骨髓树突状细胞会产生干扰素 λ 并放大干扰素 α，以应对丙型肝炎病毒感染。
DOI：
10.1053/j.gastro.2012.10.034
复制
发表时间：
2013-02
期刊：
影响因子：
29.4
通讯作者：
Szabo G
中科院分区：
文献类型：
--
作者：
Zhang S;Kodys K;Li K;Szabo G
The type III interferons (IFN-λs: interleukin [IL]-28a, IL-28b, and IL-29) have important roles in hepatitis C virus (HCV) infection, but little is understood about what cells produce these cytokines or how production is activated. We investigated whether human immune cells recognize HCV-infected cells and respond by producing IFN-λ. We cultured healthy human peripheral blood mononuclear cells (PBMCs) with different populations of immune cells and JFH-1 HCV-infected Huh7.5 (HCVcc/Huh7.5) cells. Human PBMCs recognized HCVcc/Huh7.5 cells responded by producing IFN-α, IFN-γ, and IFN-λ. A rare subset of myeloid dendritic cells (mDCs), which are BDCA3+, (also called mDC2 cells), were the major source of IL-28 and IL-29 production in response to HCVcc/Huh7.5 cells. Plasmacytoid DCs (pDCs) produced IFN-α, whereas natural killer and natural killer T cells were the main source of IFN-γ production in co-culture experiments. Of the endosomal toll-like receptors (TLRs)3, 7, 8, and 9, only TLR3 or double-stranded HCV RNA induced production of IL-28 and IL-29 by mDC2s; endosomal maturation was required. Production of IFN-α and IFN-λ were linked—IFN-λ increased production of IFN-α by pDCs and IFN-α significantly increased production of IFN-λ. mDC2s are a major source of IFN-λs production by PBMCs in response to HCVcc/Huh7.5 cells. mDC2s are activated through the TLR3 pathway, indicating that human DCs can efficiently initiate and immune response against HCV infection. IFN-λ therefore has an important role in HCV infection.
登录
查看更多内容
影响因子：
24.5
作者：
Kelly C;Klenerman P;Barnes E
通讯作者：
Barnes E
DOI：
10.1084/jem.20092140
发表时间：
2010-06-07
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Jongbloed SL;Kassianos AJ;McDonald KJ;Clark GJ;Ju X;Angel CE;Chen CJ;Dunbar PR;Wadley RB;Jeet V;Vulink AJ;Hart DN;Radford KJ
通讯作者：
Radford KJ
DOI：
10.1084/jem.20092618
发表时间：
2010-06-07
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Poulin LF;Salio M;Griessinger E;Anjos-Afonso F;Craciun L;Chen JL;Keller AM;Joffre O;Zelenay S;Nye E;Le Moine A;Faure F;Donckier V;Sancho D;Cerundolo V;Bonnet D;Reis e Sousa C
通讯作者：
Reis e Sousa C
影响因子：
13.5
作者：
Marukian, Svedana;Jones, Christopher T.;Andrus, Linda;Evans, Matthew J.;Ritola, Kimberly D.;Charles, Edgar D.;Rice, Charles M.;Dustin, Lynn B.
通讯作者：
Dustin, Lynn B.
影响因子：
13.5
作者：
Marukian, Svetlana;Andrus, Linda;Sheahan, Timothy P.;Jones, Christopher T.;Charles, Edgar D.;Ploss, Alexander;Rice, Charles M.;Dustin, Lynn B.
通讯作者：
Dustin, Lynn B.