Toll-Like Receptors in Idiopathic Orbital Inflammation

被引:7
|
作者
Wladis, Edward J. [1 ]
Iglesias, Bibiana V. [4 ]
Adam, Alejandro P. [3 ]
Nazeer, Tipu [2 ]
Gosselin, Edmund J. [1 ]
机构
[1] Albany Med Coll, Dept Ophthalmol, Lions Eye Inst, Slingerlands, NY 12159 USA
[2] Albany Med Coll, Dept Pathol, Albany, NY 12208 USA
[3] Albany Med Coll, Ctr Cell Biol & Canc Res, Albany, NY 12208 USA
[4] Albany Med Coll, Ctr Immunol & Microbial Dis, Albany, NY 12208 USA
来源
关键词
MYOSITIS; EXPRESSION; INTERLEUKIN-12; INFLIXIMAB; CELLS;
D O I
10.1097/IOP.0b013e3182565c59
中图分类号
R77 [眼科学];
学科分类号
100212 ;
摘要
Purpose: A prior investigation has demonstrated that innate immune-specific cytokines are enriched in idiopathic orbital inflammation (IOI). To further document the role of innate immunity in IOI, the authors sought to determine whether toll-like receptors (TLRs) are present in biopsy specimens of this disorder. Methods: Immunohistochemical staining for TLR2, TLR3, and TLR4 was performed on biopsy specimens taken from patients with IOI, and the number of TLR-positive cells was counted across five 40x light microscopic fields. These results were compared with an isotype control and with orbital adipose tissue taken from patients without evidence of inflammation. Results: All IOI specimens demonstrated positivity for all 3 TLRs, and sections stained for isotype controls did not demonstrate any positivity. Furthermore, orbital adipose tissue did not demonstrate any significant signal. The mean number of positive cells was 24.4 cells/high power field (hpf; standard deviation = 11.6 cells/hpf), 7.23 cells/hpf (standard deviation = 5.59 cells/hpf), and 11.7 cells/hpf for TLR2, TLR3, and TLR4, respectively. Conclusions: This study provides the first documentation of TLRs in orbital disease. Toll-like receptors are present in IOI, and IOI may represent an aberrant innate immune response. Interference with TLRs may represent an additional potential therapeutic mechanism in the management of IOI. (Ophthal Plast Reconstr Surg 2012;28:273-276)
引用
收藏
页码:273 / 276
页数:4
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