MMP-2、TIMP-1、TIMP-2在SD大鼠眼前段组织的表达

目的观察不同年龄段正常SD大鼠眼前段组织中MMP-2、TI MP-1和TI MP-2的表达,探讨正常生理状态下MMP及TI MP在小梁网房水流出及葡萄膜巩膜房水流出通道中的作用。方法应用酶免疫组化技术,检测不同年龄段正常SD大鼠眼前段组织中MMP-2、TI MP-1和TI MP-2的定位。阳性结果应用图像分析系统进行定量分析。结果免疫组化结果显示MMP-2、TI MP-1及TI MP-2分布于SD大鼠眼前段的虹膜、睫状体及小梁网。MMP-2在眼组织各部位的阳性反应强于TI MP-1及TI MP-2。随着年龄增长,MMP-2、TI MP-1及TI MP-2表达量逐渐增加,在出生后2~3月(成年期)达最高值,以后(中老年期)出现下降。结论MMP-2、TI MP-1和TI MP-2广泛分布于不同年龄段SD大鼠的小梁网房水流出及葡萄膜巩膜房水流出通道,且随着年龄变化而改变,对维持正常房水流出具有重要作用。     

体外培养猴眼小梁细胞及睫状肌细胞中组织金属蛋白酶抑制剂的表达

目的：观察体外培养的正常猴眼小梁细胞及睫状肌细胞中组织金属蛋白酶抑制剂（tissue inhibitors of metalloproteinase,TIMP)的表达,探讨生理状态下基质金属蛋白酶（matrix metalloproteinase,MMP)及TIMP在小梁网房水流出及葡萄膜－巩膜房水流出的通道中的作用。方法：采用Reverse-zymography技术,检测猴眼小梁细胞及睫状肌细胞中TIMP及MMP的表达。结果;猴眼小梁细胞及睫状肌细胞培养液中均可见TMIP－1、TIMP－2及TIMP－3表达,小梁细胞中MMP／TIMP比值明显高于睫状肌细胞。结论：正常状态下小梁细胞外基质的降解能力明显高于睫状肌细胞,可能是由于传统的小梁网房水流出通道作用强于葡萄膜－巩膜房水流出通道 的作用。     

白细胞介素-1α对猪小梁细胞基质金属蛋白酶／基质金属蛋白酶抑制剂表达的影响

背景房水外流通路的阻塞或小梁网细胞外基质（ECM）的异常堆积导致房水流畅系数降低是引起眼压升高的原因之一,基质金属蛋白酶（MMPs）和组织金属蛋白酶抑制剂（TIMPs）的平衡对ECM的代谢至关重要,白细胞介素-1α（IL-1α）可以通过调节MMPs的表达而调节房水的外流。目的研究猪重组IL-1α对体外培养的猪眼小梁细胞MMP-2、MMP-3及TIMP-1表达的影响。方法从猪眼取出带有小梁组织的巩膜,用组织块培养法培养小梁细胞并进行传代,第3代的猪小梁细胞应用纤维连接蛋白（FN）和层黏连蛋白（LM）进行鉴定。第3代小梁细胞血清饥饿培养24h后分为2组,对照组加入无血清培养基,IL组加入10m／L IL-1α,分别培养30min。采用细胞免疫化学法分析IL组MMP-2、MMP-3及TIMP-1蛋白在培养小梁细胞中的表达;采用逆转录聚合酶链反应（RT—PCR）法检测小梁细胞中MMP-2mRNA、MMP-3mRNA及TIMP-1 mRNA的表达,并与对照组的检测结果进行比较。结果传3代的细胞对FN和LM呈现阳性反应。与对照组比较,IL组小梁细胞中MMP-3和TIMP-1蛋白的表达量（A值）明显升高,差异均有统计学意义（t=-7．694、t=-5．199,P〈0．05）,但2组间小梁细胞中MMP-2表达的差异无统计学意义（t=-2．365,P〉0．05）。IL组小梁细胞中MMP-3mRNA和TIMP-1mRNA的表达量（A值）明显高于对照组,差异均有统计学意义（t=-3．025、t=-1．921,P〈0．05）,而2组间小梁细胞中MMP-2mRNA的表达差异无统计学意义（t=-1．173,P〉0．05）。结论外源性IL-1α能增加猪眼小梁细胞中MMP-3、TIMP-1的表达,引起MMP-3／TIMP-1平衡改变,促进小梁网ECM的分解,增加房水外流,而对MMP-2的表达无影响。     

IL-1α对体外培养的牛小梁网细胞MMPs及TIMPs表达的影响

目的 观察白细胞介素-1α（IL-1α）对体外培养的牛小梁网细胞分泌基质金属蛋白酶（MMPs）和基质金属蛋白酶组织抑制剂（TIMPs）的影响，探讨IL-1α降低眼压的机制。方法 采用酶谱分析法和反向酶谱分析法检测牛小梁网细胞MMP和TIMPs的分泌，并观察IL-1α对MMP和TIMPs分泌的调节作用。结果 体外培养的牛小梁细胞分泌MMP-2、MMP-3、MMP-9和TIMP-1；IL-1α对MMP-2、MMP-3、MMP-9的分泌有促进作用，且呈时间和浓度依赖性，其中以IL-1α对MMP-3的分泌促进作用最强；IL-1α对TIMP-1的分泌也有微小的增加作用。结论 IL-1α能够显著促进牛小梁网细胞分泌MMPs，打破了MMP／TIMPs的平衡，可能进一步促进小粱网细胞外基质（ECM）的分解，增强房水流动性。     

硒对体外培养的牛眼小梁细胞MMP-2和TIMP-1分泌的影响

目的:了解硒对体外培养牛眼小梁(TM)细胞基质金属蛋白酶-2(MMP-2)分泌的影响,探讨硒在原发性开角型青光眼(POAG)发病机制中的作用。方法:用含有1,2,5和10μg/L有机硒化合物(MSeA,甲基硒酸)的无血清DMEM分别孵育TM细胞,对照组(Co)加入不含实验药物的无血清DMEM分别孵育TM细胞24h,用免疫组织化学法对MMP-2进行定性和半定量检测,Western印迹法对TIMP-1进行定量检测。结果:硒化合物可减少MMP-2和TIMP-1的分泌。结论:硒通过改变MMP-2和TIMP-1的分泌,影响房水流出通路上细胞外基质之间相互转化的平衡,增加房水流出阻力,参与POAG的发病。     

猪眼小梁细胞的鉴定及压力对猪眼小梁细胞MMP-2、MMP-3及TIMP-1表达的影响

目的 探讨压力对体外培养的猪眼小梁细胞基质金属蛋白酶-2(matrix metalloproteinases,MMP-2)、MMP-3以及基质金属蛋白酶组织抑制剂-1(tissue inhibitors of MMPs,TIMP-1)表达的影响.方法 培养猪眼小梁细胞并进行鉴定.对传第3代的小梁细胞施加20 mmHg(1 kPa=7.5 mmHg)、40 mmHg、60 mmHg及80 mmHg压力作为实验组,0 mmHg设为对照组.培养48 h后对MMP-2、MMP-3和TIMP-1进行免疫组织化学SP法染色及电镜扫描,并对染色结果进行统计学分析.结果 根据培养细胞的生长特性、形态特征及细胞免疫组织化学染色结果等特点,确定培养的细胞为猪眼小梁细胞.猪眼小梁细胞正常可以少量表达MMP-2、MMP-3和TIMP-1.20 mmHg、40 mmHg、60 mmHg时猪眼小梁细胞MMP-2的SP染色细胞阳性率分别为(34.30±10.89)%、(47.48±4.96)%、(58.40±8.67)%,TIMP-1的SP染色细胞阳性率分别为(20.40±7.63)%、(37.66±11.64)%、(49.58±8.10)%,MMP-3的SP染色细胞阳性率分别为(12.30±4.35)%、(11.98±2.26)%、(15.24±5.63)%.因此压力改变在一定程度上可以促进猪眼小梁细胞表达MMP-2、TIMP-1,而对猪眼小梁细胞MMP-3的表达无明显影响.结论 一定范围内压力的变化可以改变MMPs/TIMPs之间的平衡状态,进而影响小梁细胞外基质细胞外基质的代谢以及房水外流阻力,因此MMPs在青光眼的发病机制中发挥重要作用.     

Unoprostone对猴睫状肌组织胶原Ⅲ、Ⅳ及MMP-1影响的免疫组化研究

目的 :探讨PGF2 α类抗青光眼药Unoprostone对猴的降眼压作用是否与睫状肌组织中细胞外基质 (Extracellularmatrix ,ECM )及基质金属蛋白酶 (Matrixmetalloproteinase ,MMP)的表达有关。方法 :1 采用免疫组织化学方法观察正常猴睫状肌、小梁网、睫状突及虹膜组织中胶原Ⅰ、Ⅲ、Ⅳ及MMP 1的分布。 2 比较Unoprostone对 7只猴点眼两周前后睫状肌前部纵行肌部分胶原Ⅲ、Ⅳ及MMP 1免疫染色变化。结果 :1 正常猴睫状肌、小梁网、睫状突及虹膜组织中胶原Ⅰ、Ⅲ、Ⅳ及MMP 1的分布各自具有不同特点。 2 Unoprostone点眼两周后实验眼眼压均下降 5mmHg以上 ,同时睫状肌前部纵行肌部分胶原Ⅲ染色减弱 (7只动物中 5只减弱 )、胶原Ⅳ染色减弱(7只动物中 6只减弱 ) ,MMP 1染色增强 (7只动物中 7只增强 )。胶原Ⅰ未见明显染色。结论 :Unoprostone对猴的降眼压作用与睫状肌组织MMP表达增强 ,引起ECM降解加强 ,从而葡萄膜巩膜房水流出增加有关。     

NF-κB对人眼小梁细胞MMP-3及TIMP-1 mRNA表达的影响

目的研究NF-κB对人眼小梁细胞基质金属蛋白酶-3（matrix metalloproteinase-3，MMP-3）及组织金属蛋白酶抑制剂-1（tissue inhibitor of metalloproteihase-1，TIMP-1）mRNA表达的影响。方法采用原代培养的人眼小梁细胞，通过脂质体转染的方法，将P65表达质粒转染小梁细胞，24h后通过RT-PCR方法检测MMP-3及TIMP—1 mRNA的表达。结果P65转染后MMP-3 mRNA的表达明显增高，与正常对照组相比差异有显著性（P〈0．05），TIMP—1 mRNA的表达与正常对照组相比无明显改变（P〉0．05）。结论NF—κB的活化可激活MMP-3的表达，提示NF-κB信号通路参与了小梁网外引流通道的调控。     

内毒素诱导性葡萄膜炎眼中NO含量和基质金属蛋白酶-9及其组织型金属蛋白酶抑制剂-1与诱导型NO合酶的表达

目的 观察基质金属蛋白酶（MMP）-9及其组织型金属蛋白酶抑制剂（TIMP）-1、一氧化氮（NO）和诱导型一氧化氮合酶（iNOS）在内毒素诱导性葡萄膜炎（EIU）眼组织中的变化。 方法 90只Sprague-Dawley(SD)大鼠随机分为实验组(81只)和对照组(9只)。实验组大鼠双后足垫注射伤寒杆菌内毒素(LPS)200 μl建立EIU模型；对照组大鼠不予注射。在LPS注射后0、6、12、18、24、48、72、96h和7d分别处死9只实验组大鼠，观察眼部改变并进行组织病理学检查。检测血浆、房水和葡萄膜组织的NO含量和房水蛋白浓度。免疫组织化学方法和计算机图像分析系统检测MMP-9、TIMP-1和iNOS的表达及其平均吸光度［A, 旧称光密度（OD）］值。 结果 虹膜、睫状体的上皮细胞和渗出的炎性细胞表达iNOS、MMP-9和TIMP-1。房水蛋白浓度，血浆、房水和葡萄膜组织中NO含量，以及MMP-9的A值与炎症程度呈正相关，iNOS和TIMP-1的A值与炎症程度无明显相关性。iNOS在LPS注射后6h可见表达，12h达高峰，以后逐渐下降。TIMP-1表达出现于24h，72h时达高峰。 结论 在EIU发生、发展过程中, MMP-9、TIMP-1、NO、iNOS的含量或表达发生变化，提示它们参与EIU的病理过程。 (中华眼底病杂志, 2005, 21: 371-374)     

Unoprostone对猴睫状肌组织胶原Ⅲ、Ⅳ及MP—1影响的免疫组化研究

目的：探讨PGF2α类抗青光眼药Unoprostone对猴的降眼压作用是否与眼状肌组织中细胞外基质（Extracellular matrix,ECM)及基质金属蛋白酶（Matrix metalloproteinase,MMP)的表达有关。方法：1．采用免疫组织化学方法观察正常猴睫状肌，小梁网，睫状突及虹膜组织中胶原I，Ⅲ，Ⅳ及MMP－1的分布。2．比较Unoprostone对7只猴点眼两周前后睫状肌前部纵行肌部分胶原，Ⅲ，Ⅳ及MMP－1免疫染色变化。结果：1．正常猴睫状肌，小梁网，睫状突及虹膜组织中胶源，I，Ⅲ，Ⅳ及MMP－1的分布各自具有不同特点。2．Unoprostone点眼两周后实验眼眼压均下降4mmHg以上，同时睫状肌前部纵行肌部分胶原Ⅲ染色减弱（7只动物中5只减弱），胶原Ⅳ染色减弱（7只动物中6只减弱），MMP－1染色增强（7只动物中7只增强），胶原I未见明显染色。结论：Unoprostone对猴的降眼压作用与睫状肌组织MMP表达增强，引起ECM降解加强，从而葡萄膜巩膜房水流出增加有关。     

Identification of the mouse uveoscleral outflow pathway using fluorescent dextran

PURPOSE: This study was undertaken to assess directly whether there is uveoscleral outflow in the mouse eye by monitoring the movement of intracamerally injected fluorescent dextran. METHODS: After anesthesia, NIH Swiss mice received intracameral injection of 1.5 microL of 0.2 pg/microL 70-kDa dextran conjugated to tetramethyl-rhodamine and to lysine. After survival times of 10, 20, 60, and 120 minutes, the experiments were terminated by transcardial perfusion with 2% paraformaldehyde. The eyes were enucleated and embedded in paraffin, and sections were prepared. These sections were then analyzed by fluorescence microscopy. RESULTS: Fluorescent tracer in the eyes of animals that survived for 10 minutes was prominent in the iris root and ciliary processes and was of moderate intensity in the adjacent sclera. Moderate intensity fluorescence also was observed in the trabecular meshwork and adjacent cornea. At 20 minutes, intense fluorescence was observed in the ciliary processes and the ciliary muscle. This fluorescence in the ciliary muscle extended from the posterior edge of the ciliary muscle's tail into the anterior choroid. At 60 minutes, the fluorescence in the choroid extended to the equator and adjacent sclera. The intensity of the fluorescence within the ciliary processes of these eyes was substantially reduced when compared with the 20-minute-survival eyes. At 120 minutes, label was observed only within trabecular meshwork and Schlemm's canal. CONCLUSIONS: These results indicate that at least a portion of aqueous outflow in the mouse eye is through the uveoscleral outflow pathway.     

Uveoscleral outflow using different-sized fluorescent tracers in normal and inflamed eyes

Sodium fluorescein and fluorescinated dextrans (FD) of selected molecular weights were combined and perfused into the anterior chamber of normal and inflamed eyes of cynomolgus monkeys. The eyes were dissected into iris, anterior and posterior uvea, anterior and posterior sclera, retina and intraocular fluids (excluding aqueous). Each tissue was homogenized and centrifuged and the supernatant was run through a gel-filtration column to separate the fluorescent tracers. Each of the resultant peaks was quantitated and facility of uveoscleral outflow was determined. In control eyes the calculated facility of uveoscleral outflow was very similar with all tracers (from 0.047-to 0.052 microliter min-1 mmHg-1) and each tracer was found in highest concentration in the anterior sclera and anterior uvea. In inflamed eyes the calculated facility of uveoscleral outflow increased two- to five-fold with each tracer (0.12-; 0.17-; 0.29-; and 0.24 microliter min-1 mmHg-1 with fluorescein, and the fluorescinated dextrans of MWs 4000, 40,000 and 150,000, respectively). Each tracer was found in the anterior sclera and uvea in inflamed eyes whereas the posterior sclera and uvea contained predominantly the higher molecular-weight tracers (MWs 40,000 and 150,000). It is concluded that iridocyclitis causes an increase in uveoscleral outflow by increasing the permeability of the anterior uvea to all tracers and fluid. Small tracers may then diffuse into uveal blood vessels or across the sclera, yielding lower values for uveoscleral outflow. Of the four tracers studied, the optimal tracer size for studying uveoscleral outflow in either normal or inflamed eyes is MW 40,000.     

Latanoprost and matrix metalloproteinase-1 in human choroid organ cultures.

PURPOSE: Latanoprost, a prostaglandin F2a analogue and ocular hypotensive agent, alters extracellular matrix and matrix metalloproteinases (MMPs), including MMP-1, within tissues of the uveoscleral outflow pathway. In addition to these tissues, the anterior choroid also is exposed to fluid within the uveoscleral outflow pathway. The present study was undertaken to compare MMP-1 expression in the choroid with other uveoscleral pathway tissues and to determine the effect of latanoprost on MMP-1 expression in human choroid organ cultures. METHODS: Choroid tissue explant cultures were generated and incubated with PhXA85, the biologically active form of latanoprost, or vehicle for 12 or 18 hours. Explant cultures from iris and ciliary body also were generated and exposed to PhXA85. Protein extracts of theses cultures, as well as from fresh tissues, were then probed for MMP-1 by Western blotting. All samples were normalized for protein content and reletive expression was evaluated by densitometry. Also, total RNA was harvested from fresh tissues or from cultures treated with PhXA85. The amount of MMP-1 mRNA in these samples was measured using real time polymerase chain reaction. These results were normalized according to simultaneous measurements of glyceraldehyde-3-phosphate dehydrogenase mRNA within the same samples. RESULTS: Compared to the ciliary body, in which specific MMP-1 concentration (/total mg protein) was greatest, the specific MMP-1 concentrations within iris, anterior choroid, and posterior choroid were less by 24.7 +/- 0.69%, 40.7 +/- 1.04%, and 64.5 +/- 0.52%, respectively (mean +/- SD). The order of MMP-1 mRNA expression among these tissues from fresh eyes was ciliary body < anterior choroid < posterior choroid < iris. Treatment of ciliary body explant cultures with 200 nM PhXA85 for 12 hours increased MMP-1 protein content by 154 +/- 34% (P = 0.004, students t test, N = 3). In contrast, similar treatment of anterior choroid, posterior choroid, or iris explant cultures minimally changed MMP-1 protein content (23 +/- 22+/-, P = 0.124; 14 +/- 8%, P = 0.462; 27 +/- 16%, P = 0.037, respectively). Increased MMP-1 was observed in choroid cultures incubated for 18 hrs with 200 nM or 500 nM PhXA85. MMP-1 mRNA in 12 hour PhXA85-treated choroid cultures was the same or less than vehicle-treated cultures from 7 of 9 donors. In contrast, MMP-1 mRNA was increased in PhXA85-treated ciliary body cultures from 2 of 2 donors. CONCLUSIONS: These results suggest that the capacity for latanoprost-mediated induction of MMP-1 within the choroid is less than within the ciliary muscle. Hence, it is unlikely that induction of MMP-1 in choroid plays as important a role in uveoscleral outflow modulation as induction of MMP-1 in the ciliary muscle.     

Effects of prostaglandins on the aqueous humor outflow pathways

Topical treatments with certain prostaglandins (PGs), including FP receptor agonists, lower intraocular pressure by increasing uveoscleral outflow. Although the precise mechanism for the increased uveoscleral outflow is not known, there appears to be activation of a molecular transduction cascade and an increase in the biosynthesis of certain metalloproteinases. This leads to reduction of extracellular matrix components within the ciliary muscle, iris root, and sclera. It is possible that this reduction of extracellular matrix present within portions of the uveoscleral pathway may contribute to the mechanism of increased uveoscleral outflow. Additional mechanisms that may contribute to the PG-mediated increase of uveoscleral outflow include relaxation of the ciliary muscle, cell shape changes, cytoskeletal alteration, or compaction of the extracellular matrix within the tissues of the uveoscleral outflow pathway. Future studies should clarify the importance of these various responses that may contribute to increased uveoscleral outflow. At present, there is no compelling evidence for a substantial facility-increasing effect on the trabecular meshwork outflow for any of these compounds.     

Immunosuppressive properties of tissues of the ocular anterior segment

To determine whether explants of various tissues comprising the anterior segment of individual normal eyes can display immunosuppressive properties in vitro, explants of iris/ciliary body, cornea, cornea-limbus, sclera and conjunctiva were prepared from single eyes of BALB/c mice and tested for their capacity to suppress alloantigen-driven T cell activation in vitro. Cultured explants of iris and ciliary body, and of cornea, but not sclera or conjunctiva, suppressed T cell activation in vitro. Similarly, the supernatants of cultured iris/ciliary body and cornea explants displayed immunosuppressive properties. Prostaglandins appeared to make a minor contribution to the inhibition observed. The authors conclude that certain tissues within the anterior segment of the eye (iris, ciliary body, cornea) contain cells that secrete immunosuppressive factors, whereas other tissues (conjunctiva, sclera) lack this feature. The secretions of the former tissues undoubtedly contribute to the immunosuppressive features of the microenvironment in the anterior segment of the eye, and help to account for the existence of immune privilege.     

非穿透性小梁手术对葡萄膜巩膜房水流出量的影响

目的探讨非穿透性小梁手术（nonpenetrating trabecular surgery，NPTS）对葡萄膜巩膜房水流出量的影响，从房水动力学的角度揭示NPTS降眼压的机制。方法用示踪剂异硫氰酸荧光素牛血清白蛋白（fluoresceinisothiocyanate—bovine serum albumin：FITC—BSA）于术后7d分别对手术后的兔眼模型组和正常兔眼组进行前房持续灌注30min，灌注毕处死家兔，摘除双侧眼球，并将组织分离为前巩膜、后巩膜、前葡萄膜、后葡萄膜、视网膜和残余液体等6种组织。测定每种组织的荧光强度，计算葡萄膜巩膜流出量（uveoscleral outflow，Fu）。结果实验组葡萄膜巩膜流出量明显高于正常组，两组前房水再现量均以前葡萄膜、前巩膜和残余液体为多，实验组术后葡萄膜巩膜通道各组织房水再现量与正常组相比差异有统计学意义（p〈0．001）。结论非穿透性小梁手术能增加葡萄膜巩膜途径房水流出量，房水主要由前巩膜排出。     

Light and electron microscopy of the anterior chamber angle structures following surgical disinsertion of the ciliary muscle in the cynomolgus monkey.

Light and electron microscopic studies were done on 11 cynomolgus monkey eyes which had undergone total iris removal followed by surgical disinsertion of the ciliary muscle from the scleral spur 4.7 to 14.4 months earlier. Anterior chamber perfusion to measure gross outflow facility had been performed one to nine times postoperatively. Over most of the circumference in most eyes (1) the ciliary muscle had been retrodisplaced from the scleral spur and had reattached to the sclera more posteriorly; (2) ciliary muscle, trabecular meshwork, and Schlemm's canal appeared normal. A cyclodialysis cleft was never seen. Fixation of some eyes in the in vivo and in vitro presence of pilocarpine demonstrated the contractibility of the retrodisplaced muscle. In isolated areas where the ciliary body had been surgically cut, scar tissue of varying thickness connected scleral spur, sclera, ciliary body, zonule, and lens capsule, but did not infiltrate trabecular meshwork or Schlemm's canal. In such sectors, plasma cell-like cells replaced trabecular endothelial cells and were also present in the scar tissue, ciliary muscle, and surrounding vessel walls in the scar and sclera. In sectors of two eyes, a previously existing trabecular operculum extended posteriorly and completely covered the meshwork. The meshwork in these sectors was poorly perfused by aqueous humor, and electron-dense deposits were present beneath the inner wall of Schlemm's canal. Four totally iridectomized and two unoperated eyes from these monkeys were also examined; ciliary muscle, trabecular meshwork, and Schlemm's canal appeared normal in all, despite the numerous anterior chamber perfusions.     

Distinctive distribution of HLA class II presenting and bone marrow derived cells in the anterior segment of human eyes.

Cells of bone marrow origin that normally occupy the stroma of the murine iris and ciliary body have been implicated in the immune phenomenon, anterior chamber associated immune deviation (ACAID). Following injection of antigen into the anterior chamber, cells of this type deliver an ACAID inducing signal into the systemic circulation, presumably through the outflow tract. In an effort to identify such cells in man, anterior chambers of 34 human donor eyes of different age groups were stained immunocytochemically with monoclonal antibodies directed at HLA class II molecules, CD 45 (a molecular marker of bone marrow-derived cells) and macrophage-associated membrane molecules (CD 68, CD 14). Within the outflow tissue, the cells of the filtering trabecular meshwork stained with none of those reagents. However, infrequent single, dispersed, dendritic cells were positively stained in the intertrabecular spaces. More numerous labelled cells were found in the anterior- and posterior-most portions of the non-filtering part of the trabecular meshwork. These cells were continuous with stained cells adjacent to the outer wall of Schlemm's canal and to the collector channels. Numerous labelled cells were seen in the vicinity of the intra- and episcleral vessels, the ciliary meshwork, the stroma of the ciliary muscle and epithelial processes, and the iris stroma. With advancing age, increasing numbers of CD 45+, HLA class II expressing cells appeared to accumulate in the so-called uveoscleral pathway. These results indicate that bone marrow-derived cells with the potential to function of ACAID induction reside within human eyes, and that cells of this type are located not only in the stroma of iris and ciliary body, but within the non-filtering portions of the trabecular meshwork and the uveoscleral pathway. The appearance of rare CD 45+ cells "in transit" in the filtering trabecular meshwork is compatible with the view that cells carrying ACAID-inducing signals to the systemic immune apparatus escape from the eye by this route.     

Formation and drainage of aqueous humor following total iris removal and ciliary muscle disinsertion in the cynomolgus monkey.

Aqueous humor formation (AHF), uveoscleral flow (U), gross outflow facility (Cg), true facility of outflow from the anterior chamber (Ct1), true facility of outflow from anterior chamber into the general circulation (Ct2), and the pressure sensitivity of AHF (pseudofacility; Cps) were determined in cynomologus monkey eyes which had undergone total iris removal or iris removal followed by ciliary muscle disinsertion. AHF was in the normal range in iridectomized-only eyes. AHF was present but reduced in "disinserted" eyes. U was markedly reduced and similar in both types of eyes. Cps was normal and Cg, Ct1, and Ct2 were low in "disinserted" eyes. Cg, Ct1, and Ct2 were nearly equal in the "disinserted" eyes, indicating that gross facility consisted almost entirely of pressure-dependent flow from anterior chamber into the general circulation, presumably via the conventional drainage routes.