Human plasmacytoid dendritic cell accumulation amplifies their type 1 interferon production.
Human plasmacytoid dendritic cell accumulation amplifies their type 1 interferon production.
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DOI：
10.1016/j.clim.2010.02.014
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发表时间：
2010-07
期刊：
影响因子：
--
通讯作者：
Greenberg SA
中科院分区：
文献类型：
--
作者：
Liao AP;Salajegheh M;Morehouse C;Nazareno R;Jubin RG;Jallal B;Yao Y;Greenberg SA
为了确定在几种自身免疫性疾病中观察到的浆细胞样树突状细胞（pDC）在组织部位积聚的潜在后果，我们测量了循环人类pDC中1型干扰素的产生与pDC浓度的关系。测定干扰素α和阻断1型干扰素受体（IFNAR）对人pDC 1型干扰素及干扰素诱导的转录和蛋白产生的影响。通过依赖ifnar的机制，人类pDCs在浓度超过血液中正常水平的情况下更有效地产生干扰素- α。细胞外干扰素- α增加了1型干扰素的pDC生成。pDCs在病变组织部位的积累使得局部1型干扰素产生显著的非线性扩增。依赖ifnar的人pDCs产生干扰素的机制的作用比以前认为的要大。IFNAR阻断具有减少所有人类细胞产生1型干扰素的潜力。
To determine the potential consequences of plasmacytoid dendritic cell (pDC) accumulation in tissue sites observed in several autoimmune diseases, we measured type 1 interferon production from circulating human pDCs as a function of pDC concentration. The effects of interferon-alpha and blockade of the type 1 interferon receptor (IFNAR) on human pDC type 1 interferon and interferon-inducible transcription and protein production were measured. Human pDCs became far more efficient producers of interferon-alpha at concentrations beyond those normally present in blood, through an IFNAR-dependent mechanism. Extracellular interferon-alpha increased pDC production of type 1 interferons. The accumulation of pDCs in diseased tissue sites allows marked non-linear amplification of type 1 interferon production locally. The role of the IFNAR-dependent mechanism of interferon production by human pDCs is greater than previously suggested. IFNAR blockade has potential for diminishing type 1 interferon production by all human cells.
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