Mo Jun-Song, Streilein J Wayne
The Schepens Eye Research Institute, Harvard Medical School, Boston, MA, USA.
Ocul Immunol Inflamm. 2005 Apr-Jun;13(2-3):139-47. doi: 10.1080/09273940490912489.
To examine the effects of intravitreal Mycobacteria tuberculosa adjuvant (MTA) on ocular immune privilege.
MTA was injected into the vitreous cavity of BALB/c mouse eyes to induce anterior uveitis. The inflamed eyes were then examined for their capacity to afford immune privilege to injected allogeneic tumor cells and to promote anterior chamber-associated immune deviation (ACAID). Aqueous humor (AqH) was tested for IL-12 content and for its ability to inhibit T-cell activation.
AqH removed from MTA-inflamed eyes at 6 and 12 h contained high levels of IL-12, which then fell almost to baseline at 24 h. This is relevant to the finding that the inflamed eye failed to support ACAID induction at an early time period and then regained the ACAID-induction capability at a later time. Nonetheless, AqH removed from MTA-inflamed eyes retained its capacity to suppress T-cell activation, and MTA-inflamed eyes afforded extended survival to alloantigenic tumor cells implanted into the anterior chamber.
Intraocular inflammation evoked by MTA causes the local accumulation of IL-12 and simultaneously robs the eye of its capacity to promote systemic immune tolerance to eye-derived antigens. However, MTA-inflamed eyes retain immune privilege, as indicated by their support of the progressive growth of allogeneic tumor cells.
研究玻璃体内注射结核分枝杆菌佐剂(MTA)对眼免疫赦免的影响。
将MTA注入BALB/c小鼠眼玻璃体内以诱发前葡萄膜炎。然后检查炎症眼赋予注射的同种异体肿瘤细胞免疫赦免以及促进前房相关免疫偏离(ACAID)的能力。检测房水(AqH)中的IL-12含量及其抑制T细胞活化的能力。
在6小时和12小时从MTA诱发炎症的眼中取出的房水含有高水平的IL-12,然后在24小时时几乎降至基线水平。这与以下发现相关:炎症眼在早期未能支持ACAID诱导,而在后期恢复了ACAID诱导能力。尽管如此,从MTA诱发炎症的眼中取出的房水仍保留其抑制T细胞活化的能力,并且MTA诱发炎症的眼使植入前房的同种异体肿瘤细胞的存活期延长。
MTA诱发的眼内炎症导致IL-12在局部积聚,同时使眼丧失促进对眼源性抗原的全身免疫耐受的能力。然而,MTA诱发炎症的眼保留免疫赦免,这表现为它们支持同种异体肿瘤细胞的渐进性生长。