Department of Ophthalmology, Third Hospital of Hebei Medical University, 139 Ziqiang Road, Shijiazhuang, 050051, China.
Jpn J Ophthalmol. 2011 Sep;55(5):558-564. doi: 10.1007/s10384-011-0060-0. Epub 2011 Jul 20.
The aqueous humor (AH) contains numerous immunosuppressive molecules that contribute to the ocular immune privilege. Here, we mimic an inflammatory environment to analyze the inhibitory effects of the AH on lipopolysaccharide (LPS)-induced maturation of dendritic cells (DC).
Different concentrations of AH were added to dendritic cell cultures together with LPS. Dendritic cell surface markers CD80, CD86, and MHC-II were assessed by use of flow cytometry. Endocytic capability and mixed lymphocyte reaction were measured as functional maturation.
AH inhibited LPS-induced DC maturation, resulting in down-regulated expression of CD80, CD86, MHC-II, enhancement of endocytic capacity, and reduced T cell activation. Neutralizing transforming growth factor beta 2 (TGF-β(2)) in AH can totally reverse the inhibitory effect. Treatment with prostaglandin E2 (PGE(2)) antagonist alone had no effect on DC maturation. However, blocking of both TGF-β(2) and PGE(2) in the AH resulted in synergistic suppression of the inhibiting effect of AH.
These results reveal that TGF-β(2) in the AH is of crucial importance in maintaining DC in the immature state. Further experiments will clarify the immune role of PGE(2) in AH.
房水（AH）中含有多种免疫抑制分子，有助于眼部免疫豁免。在此，我们模拟炎症环境，分析 AH 对脂多糖（LPS）诱导的树突状细胞（DC）成熟的抑制作用。
将不同浓度的 AH 与 LPS 一起加入树突状细胞培养物中。通过流式细胞术评估树突状细胞表面标志物 CD80、CD86 和 MHC-II 的表达。通过吞噬能力和混合淋巴细胞反应来测量功能成熟。
AH 抑制 LPS 诱导的 DC 成熟，导致 CD80、CD86、MHC-II 的表达下调，内吞能力增强，T 细胞活化减少。AH 中的转化生长因子-β2（TGF-β2）中和抗体可完全逆转抑制作用。单独用前列腺素 E2（PGE2）拮抗剂处理对 DC 成熟没有影响。然而，AH 中 TGF-β2 和 PGE2 的双重阻断导致 AH 抑制作用的协同抑制。
这些结果表明，AH 中的 TGF-β2 对维持 DC 的未成熟状态至关重要。进一步的实验将阐明 PGE2 在 AH 中的免疫作用。
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