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首页> 外文期刊>Blood: The Journal of the American Society of Hematology >Ligand of scavenger receptor class A indirectly induces maturation of human blood dendritic cells via production of tumor necrosis factor-alpha.
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Ligand of scavenger receptor class A indirectly induces maturation of human blood dendritic cells via production of tumor necrosis factor-alpha.

机译：清道夫受体A类的配体通过产生肿瘤坏死因子-α间接诱导人血树突状细胞成熟。

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摘要

Dendritic cells (DCs) are the most potent antigen-presenting cells for naive T cells. In this study, scavenger receptor class A type I and type II (SR-A) were shown to be expressed by peripheral blood DCs (PBDCs) and monocyte-derived DCs (MDDCs). In addition, the binding of anti-SR-A antibody to these cells was lower in the presence of fucoidan, an SR-A agonist. Treatment of these DCs with fucoidan or anti-SR-A antibody markedly increased the surface expression of costimulatory molecules CD83 and major histocompatibility complex class II on the CD11c(high)CD123(low) myeloid subset of PBDCs. Furthermore, fucoidan-treated PBDCs produced tumor necrosis factor-alpha (TNF-alpha) but not IL-12p70. In addition, fucoidan-induced maturation was eliminated by pretreatment with TNF-alpha-neutralizing antibody. Finally, interferon-gamma secretion and T-cell proliferation were enhanced by coculture of T cells with fucoidan-matured PBDCs. Specific inhibitors of p38 MAPK and glycogen synthase kinase 3 suppressed TNF-alpha production and maturation of fucoidan-treated PBDCs. Moreover, MDDCs lacking SR-A failed to up-regulate CD83 expression, TNF-alpha production, and phosphorylation of p38 MAPK and glycogen synthase kinase 3-beta in the presence of fucoidan. Taken together, these results suggest that ligation of SR-A leads to induction of TNF-alpha, which subsequently induces PBDC maturation, thereby leading to enhanced T-cell stimulatory capacity.
机译：树突状细胞（DC）是幼稚T细胞中最有效的抗原呈递细胞。在这项研究中，I类清道夫受体I和II型（SR-A）被证明由外周血DC（PBDC）和单核细胞衍生的DC（MDDC）表达。另外，在岩藻依聚糖（SR-A激动剂）的存在下，抗SR-A抗体与这些细胞的结合较低。用岩藻依聚糖或抗SR-A抗体处理这些DC明显增加了共刺激分子CD83和PBDC的CD11c（高）CD123（低）髓样亚型上主要的组织相容性复合体II类的表面表达。此外，岩藻依聚糖处理的PBDC产生肿瘤坏死因子-α（TNF-alpha），但不产生IL-12p70。另外，通过用TNF-α中和抗体预处理消除了岩藻依聚糖诱导的成熟。最后，通过将T细胞与岩藻依聚糖成熟的PBDCs共培养来增强干扰素-γ的分泌和T细胞的增殖。 p38 MAPK和糖原合酶激酶3的特异性抑制剂抑制了岩藻依聚糖处理的PBDC的TNF-α产生和成熟。此外，缺少SR-A的MDDC在存在岩藻依聚糖的情况下，无法上调CD83表达，TNF-α的产生以及p38 MAPK和糖原合酶激酶3-β的磷酸化。综上所述，这些结果表明SR-A的连接导致TNF-α的诱导，其随后诱导PBDC成熟，从而导致增强的T细胞刺激能力。

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