Regulation of interphotoreceptor retinoid-binding protein (IRBP)-specific Th1 and Th17 cells in anterior chamber-associated immune deviation (ACAID).
Regulation of interphotoreceptor retinoid-binding protein (IRBP)-specific Th1 and Th17 cells in anterior chamber-associated immune deviation (ACAID).
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DOI：
10.1167/iovs.09-3389
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发表时间：
2009-12
影响因子：
4.4
通讯作者：
Kaplan HJ
中科院分区：
文献类型：
--
作者：
Cui Y;Shao H;Sun D;Kaplan HJ
前房内（前房）注射抗原可抑制迟发型超敏反应的发生，这种现象称为前房相关免疫偏离（ACAID）。作者研究了前房内注射感光细胞间类维生素A结合蛋白（IRPB）肽对IFN-γ+和IL-17+致病性T细胞发育的影响。将致葡萄膜炎（IRBP 1 -20）或非致葡萄膜炎（IRBP 161 -180）肽注射到B6小鼠的前房（AC）中。7天后，用佐剂中的致病剂量的IRBP 1 -20致敏小鼠。13天后，比较从处理和未处理小鼠的脾脏分离的T细胞的致病活性，并通过细胞内染色评估Th 1和Th 17 T细胞的数量。通过抗体染色和功能测定评估调节性T细胞活性。作者还比较了眼内注射对不同部位（包括前房、玻璃体腔和视网膜下腔）EAU的抑制作用。眼内注射眼色素原性肽（IRBP 1 -20），而非眼色素原性肽（IRBP 161 -180），可抑制IFN-γ+和IL-17+眼色素原性T细胞的产生和实验性自身免疫性葡萄膜炎（EAU）的发展。AC施用IRBP 1 -20而不是IRBP 161 -180显著降低了随后用IRBP 1 -20全身免疫后循环γδ T细胞的数量。γδ T细胞群的缺乏阻止了ACAID的发展。将葡萄膜生成肽注射到AC中通过调节Th 1和Th 17 IRBP特异性T细胞来抑制EAU的发展。循环γδ T细胞群减少，并与IL-17+葡萄膜原性T细胞活化减少相关。
Intracameral (anterior chamber) injection of antigen inhibits the development of delayed-type hypersensitivity, a phenomenon known as anterior chamber-associated immune deviation (ACAID). The authors investigated the effect of intracameral injection of interphotoreceptor retinoid-binding protein (IRPB) peptides on the development of IFN-γ+ and IL-17+ pathogenic T cells. A uveitogenic (IRBP1–20) or nonuveitogenic (IRBP161–180) peptide was injected into the anterior chamber (AC) of B6 mice. Seven days later, the mice were primed with a pathogenic dose of IRBP1–20 in adjuvant. Thirteen days later, the pathogenic activity of the T cells isolated from the spleens of treated and untreated mice were compared, and the numbers of Th1 and Th17 T cells were assessed by intracellular staining. Regulatory T-cell activity was assessed by antibody staining and functional assays. The authors also compared the effect of inhibition on EAU of ocular injection to various sites, including the AC, the vitreous cavity, and the subretinal space. Intraocular injection of the uveitogenic peptide (IRBP1–20), but not the nonuveitogenic peptide (IRBP161–180), inhibited the generation of IFN-γ+ and IL-17+ uveitogenic T cells and the development of experimental autoimmune uveitis (EAU). AC administration of IRBP1–20, but not IRBP161–180, significantly decreased the number of circulating γδ T cells after subsequent systemic immunization with IRBP1–20. Absence of the γδ T-cell population prohibited the development of ACAID. Injection of a uveitogenic peptide into the AC inhibited the development of EAU by regulation of Th1 and Th17 IRBP-specific T cells. The circulating γδ T-cell population was reduced and was associated with decreased activation of IL-17+ uveitogenic T cells.
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影响因子：
64.8
作者：
Bettelli, E;Carrier, YJ;Kuchroo, VK
通讯作者：
Kuchroo, VK
DOI：
10.4049/jimmunol.181.7.4791
发表时间：
2008-10-01
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Grajewski RS;Hansen AM;Agarwal RK;Kronenberg M;Sidobre S;Su SB;Silver PB;Tsuji M;Franck RW;Lawton AP;Chan CC;Caspi RR
通讯作者：
Caspi RR
影响因子：
4.4
作者：
Peng, Yong;Han, Gencheng;Sun, Deming
通讯作者：
Sun, Deming
影响因子：
15.3
作者：
STREILEIN, JW;NIEDERKORN, JY
通讯作者：
NIEDERKORN, JY
影响因子：
4.6
作者：
Thurau, SR;Chan, CC;Caspi, RR
通讯作者：
Caspi, RR