ライフサイエンスコーパス: RPE

1 RPE cells differentiated from these hiPSCs contained mor

2 RPE cells play critical roles in the maintenance of phot

3 RPE dysfunction plays a significant role in retinal dege

4 RPE dysfunction, especially impairment of its phagocytic

5 RPE humps on structural OCT were identified in 99 out of

6 RPE humps were defined as RPE elevations above its physi

7 RPE migration was detected in 52 of 155 eyes (33.5%) and

8 RPE phagocytosis helps maintain the viability of photore

9 Among those aged </=45, RPE-BM was significantly thicker among those of black or

10 ersistent subretinal fluid (SRF), but also a RPE-independent visual cycle for cone photopigment withi

11 HB production was observed in the Abca4(-/-) RPE, in which loss of the ATP-binding cassette A4 transp

12 Finally, in aged RPE cells, TSPO expression was reduced and cholesterol e

13 real injection of IL-4 and IL-10 ameliorated RPE toxicity that was induced by NaIO3Ex vivo coculture

14 We sought to understand why a defect in an RPE ion-channel result in abnormal electrophysiology at

15 absence of scrolled RPE or other signs of an RPE tear.

16 Cases were defined as eyes in which an RPE tear developed during treatment.

17 m to contribute to the regulation of BRB and RPE permeability by vasoinhibins under diabetic or hyper

18 E-19, cultured murine primary RPE cells, and RPE samples from live mice.

19 Drusen and RPE changes were seen in the peripheral retina, anterior

20 or cystoid spaces, hyperreflective foci, and RPE layer atrophy or absence.

21 involvement of the outer retinal layers and RPE.

22 f metabolites between the photoreceptors and RPE because photoreceptor cells have very high energy de

23 i.e., the contact between photoreceptors and RPE) is the primary site of inflammation in ARPE.

24 Patient podocytes and RPE cells carrying disease-associated CFH genetic varian

25 L, mGCC, mGCL-IPL, mINL, mOPL, mONL, PR, and RPE parameters and total retinal thicknesses between gro

26 ogy, normal morphology of outer segments and RPE cells, and no evidence of photoreceptor degeneration

27 segment loss, RPE drusen complex volume, and RPE drusen complex abnormal thinning volume.

28 RPE humps were defined as RPE elevations above its physiologic profile, without an

29 ion of dopaminergic RPEs and that attenuated RPEs in previous reports may reflect downstream effects

30 m media bathing either apical or basolateral RPE surfaces, and two subpopulations of small EVs includ

31 riates and to identify relationships between RPE-BM thickness and ocular and systemic features.

32 ression showed an intact association between RPEs and happiness in a computational model of momentary

33 Beside GA and characteristic RPE-tears, another atypical form of RPE-defect with over

34 d reflectivity of the pixels in the choroid, RPE band, and overlying vitreous to be quantified.

35 istologic candidates were proposed: complete RPE and outer retinal atrophy (cRORA), incomplete RPE an

36 In conclusion, RPE cells consume multiple nutrients, including glucose

37 In contrast, RPE-BM was significantly thicker among black or mixed/ot

38 strikingly, phagocytosis of POS by cultured RPE cells was almost completely blocked by pharmacologic

39 b-retinal pigment epithelium (RPE) deposits, RPE atrophy, choroidal neovascularisation and photorecep

40 The hiPSC-derived RPE cells produce several AMD/drusen-related proteins, a

41 erent experimental models: the human-derived RPE-like cell line ARPE-19, cultured murine primary RPE

42 induced-pluripotent stem cell (iPSC)-derived RPE cells, particularly with regard to the complement pa

43 , Saini et al. (2017) show that iPSC-derived RPE cells from age-related macular degeneration patients

44 DISCUSSION: RPE humps were frequently observed in highly myopic eyes

45 asal lamina band correlated with dissociated RPE.

46 a cornerstone in understanding how dopamine RPEs could drive associative learning.

47 es not affect the expression of dopaminergic RPEs and that attenuated RPEs in previous reports may re

48 hat modulate RPE tight junctions and enhance RPE barrier function.

49 stes of Mertk (-/-) mice it fails to enhance RPE phagocytosis or prevent photoreceptor degeneration.

50 tly developed a retinal pigment ephithelium (RPE)-choroid preparation to monitor the circadian clock

51 we infected the retinal pigment epithelial (RPE) cell line, ARPE-19, with cell-associated VZV and co

52 hesized in human retinal pigment epithelial (RPE) cells that are oxygenated derivatives of VLC-PUFAs,

53 ndition by using retinal pigment epithelial (RPE) cells, which are a crucial component of the outer b

54 al microvilli of retinal pigment epithelial (RPE) cells.

55 h subretinal/sub-retinal pigment epithelial (RPE) hemorrhage related to neovascular AMD (odds ratio 1

56 tina in-vivo and retinal-pigment-epithelial (RPE) cells in-vitro.

57 o lysosomes of retinal pigmented epithelial (RPE) cells acts to clear this harmful enzyme from the ex

58 ng produced by retinal pigmented epithelial (RPE) cells under different conditions simulating risk fa

59 he occurrence of retinal pigment epithelium (RPE) abnormalities, choroidal neovascularization, acquir

60 sits between the retinal pigment epithelium (RPE) and Bruch's membrane on SD-OCT, and 2) hard, puncta

61 sfunction of the retinal pigment epithelium (RPE) and dysregulation of complement have been implicate

62 function of the retinal pigment epithelium (RPE) and it is essential for retinal homeostasis.

63 elial cells, the retinal pigment epithelium (RPE) and podocytes, respectively.

64 the choroid and retinal pigment epithelium (RPE) as well as the inner retinal surface all were segme

65 d atrophy of the retinal pigment epithelium (RPE) associated with ORT on spectral-domain (SD) optical

66 an occur without retinal pigment epithelium (RPE) atrophy and that atrophy can undergo an evolution o

67 pical aspects of retinal pigment epithelium (RPE) cells and contributes to a delayed c-wave response.

68 uller cells, and retinal pigment epithelium (RPE) cells and were visualized using confocal microscopy

69 migration of the retinal pigment epithelium (RPE) cells in age-related macular degeneration (AMD) usi

70 tion beneath the retinal pigment epithelium (RPE) cells is supposed to contribute the pathogenesis of

71 endothelium and retinal pigment epithelium (RPE) components of the BRB, and that TRPV4-selective ant

72 atypical central retinal pigment epithelium (RPE) defects not attributable to geographic atrophy (GA)

73 by extensive sub-retinal pigment epithelium (RPE) deposits, RPE atrophy, choroidal neovascularisation

74 ells to generate retinal pigment epithelium (RPE) from an individual suffering from retinitis pigment

75 the presence of retinal pigment epithelium (RPE) humps in high myopia, and to describe the distincti

76 localized to the retinal pigment epithelium (RPE) in Abca4 (-/-) Stargardt model mice compared to the

77 Daily, the retinal pigment epithelium (RPE) ingests a bolus of lipid and protein in the form of

78 thology involves retinal pigment epithelium (RPE) injury associated with immune cell infiltration, th

79 l retina and the retinal pigment epithelium (RPE) is critical for several processes, including visual

80 lective foci and retinal pigment epithelium (RPE) layer atrophy or absence, followed by choroid thick

81 and the area of retinal pigment epithelium (RPE) loss from the FAF.

82 increased in the retinal pigment epithelium (RPE) of age-related macular degeneration (ARMD) patients

83 age by different retinal pigment epithelium (RPE) phenotypes in the DPED surface; frequency and origi

84 investigate when retinal pigment epithelium (RPE) tears occur and their associated treatment patterns

85 eters, including retinal pigment epithelium (RPE) thickness, central macular thickness, and integrity

86 function of the retinal pigment epithelium (RPE) to support the neural retina.

87 rmally appearing retinal pigment epithelium (RPE) were the loss of the POS and ellipsoid zone associa

88 AMD) affects the retinal pigment epithelium (RPE), a cell monolayer essential for photoreceptor survi

89 photoreceptors, retinal pigment epithelium (RPE), and underlying choriocapillaris.

90 eptor-supporting retinal pigment epithelium (RPE), especially in a zone corresponding to the apices o

91 aturation of the retinal pigment epithelium (RPE), fenestrated choroid endothelial cells (ECs) and Br

92 pigments in the retinal pigment epithelium (RPE), increased oxidative stress, augmented complement a

93 entire eye, the retinal pigment epithelium (RPE), or the vascular endothelium.

94 mic factors with retinal pigment epithelium (RPE)-Bruch's membrane (BM) complex thickness as measured

95 [SD 4.65]), and retinal pigment epithelium (RPE)-related dystrophies (OR low myopia 2.7; P = .001; O

96 in (CM), and the retinal pigment epithelium (RPE).

97 nsition (EMT) of retinal pigment epithelium (RPE).

98 is of OSs by the retinal pigment epithelium (RPE).

99 volvement of the retinal pigment epithelium (RPE).

100 eneration of the retinal pigment epithelium (RPE).

101 hickening of the retinal pigment epithelium (RPE)/Bruch's complex (Bc).

102 hicken embryonic retinal pigment epithelium (RPE)/choroid in the absence of light.

103 ors (PR), and retinal pigmentary epithelium (RPE).

104 aracterized by retinal pigmented epithelium (RPE) death; the RPE also exhibits DICER1 deficiency, res

105 nctions of the retinal pigmented epithelium (RPE) is the clearance of shed photoreceptor outer segmen

106 pe Mfrp to the retinal pigmented epithelium (RPE) of Mfrp (rd6) /Mfrp (rd6) mice via adeno-associated

107 cells and the retinal pigmented epithelium (RPE).

108 in the mature retinal pigmented epithelium (RPE).

109 stress paradigm on reward prediction error (RPE) signaling in the ventral striatum.

110 mine neurons signal reward prediction error (RPE), or actual minus expected reward.

111 a prediction was ("reward prediction error," RPE).

112 both decisions and reward prediction errors (RPE) in the absence of choice violate the independence o

113 c process in which reward prediction errors (RPEs) are used to update expected values of choice optio

114 ts in representing reward prediction errors (RPEs), which are the difference between experienced and

115 2) is strongly expressed in slowly expanding RPE and CM compartments, and the loss of mouse Nf2 cause

116 In all eyes, RPE humps corresponded to large choroidal vessels liftin

117 ium following ingestion of OS by human fetal RPE and ARPE19 cells cultured on Transwell inserts.

118 metabolite transport in cultured human fetal RPE.

119 proximity to the double layers of flattened RPE detachment.

120 In general, RPE abnormalities paralleled photoreceptor degeneration,

121 stem cell-retinal pigment epithelium (hiPSC-RPE) derived from patients with three dominant MDs, Sors

122 both control (unaffected) and patient hiPSC-RPE cells.

123 plement genes was also seen in patient hiPSC-RPE cultures of all three MDs (SFD, DHRD, and ADRD).

124 Importantly basal deposits in patient hiPSC-RPE cultures were more abundant and displayed a lipid- a

125 ECM isolated from control vs. patient hiPSC-RPE cultures.

126 ion of drusen-like deposits in patient hiPSC-RPE cultures.

127 a novel autocrine/paracrine pro-homeostatic RPE cell signaling that aims to sustain photoreceptor ce

128 in in co-transfection experiments in a human RPE cell line.

129 In cultured human RPE cell line ARPE-19, expression of extrinsic JN up-reg

130 Using human RPE (ARPE-19) cell monolayers and endothelial cell syste

131 developed and tested in the vitreous humor, RPE cell homogenates and intact RPE cells.

132 To decipher the role of ERK1/2 in RPE cells, we conditionally disrupted the Erk1 and Erk2

133 detergent-insoluble ferritin accumulates in RPE cells and correlates temporally with microglial acti

134 rm of retinal lipofuscin that accumulates in RPE lysosomes and drives the pathogenesis of Stargardt m

135 MPO also disrupts lysosomal acidification in RPE cells, which coincides with nuclear translocation of

136 Indeed, knockout of AMPK in RPE cells using Clustered Regularly Interspaced Palindro

137 a) induction of complement factor B (CFB) in RPE cells.

138 We demonstrate in RPE cells that TSPO specific ligands promoted cholestero

139 earch for additional roles of choroid ECs in RPE physiology and disease.

140 suppress TNF-alpha-induced CFB expression in RPE cells in an AMPK-independent mechanism, and could be

141 Surprisingly, upregulation of ferritin in RPE cells by exogenous iron in-vitro stimulated the rele

142 ese findings suggest possible roles of JN in RPE molecular transport, phagocytosis and formation of o

143 To clarify the role of miRNAs in RPE cells, we used two different mature RPE cell-specifi

144 tion protein expression, and permeability in RPE cells.

145 o the pathological abnormalities reported in RPE cells studied from post-mortem tissues of affected m

146 ific ligands or by overexpression of TSPO in RPE cells.

147 Electrophysiological variability in RPE surprise correlated primarily with activity in regio

148 Electrophysiological variability in RPE valence correlated with activity in regions of the h

149 nd outer retinal atrophy (cRORA), incomplete RPE and outer retinal atrophy, complete outer retinal at

150 We induced RPE injury pharmacologically and genetically in transgen

151 reous humor, RPE cell homogenates and intact RPE cells.

152 duals with moderate depression showed intact RPE signals in ventral striatum (z = 3.16; P = .002) tha

153 Interestingly, RPE-specific up-regulation in the expression of several

154 ll-trans-ROL uptake from photoreceptors into RPE cells through an as yet undefined mechanism.

155 verall, our results showed that intraretinal RPE migrations occurred in various AMD stages, and that

156 d hypoxia-induced expression of CL-11 in iPS-RPE cells, and in the extracellular fluid.

157 deposits, photoreceptor outer segment loss, RPE drusen complex volume, and RPE drusen complex abnorm

158 s in RPE cells, we used two different mature RPE cell-specific Cre recombinase drivers to inactivate

159 Mean RPE-BM thickness was 26.3 mum (standard deviation, 4.8 m

160 lts from a nonsense variant and so the MERTK-RPE cells were subsequently treated with two translation

161 The volume of the migrated RPE cluster in serous PED was significantly correlated w

162 triggering Rho GTPase signals that modulate RPE tight junctions and enhance RPE barrier function.

163 efects in phagosome maturation using a mouse RPE explant model.

164 he PER2::LUC bioluminescence rhythm in mouse RPE-choroid.

165 y disrupted the Erk1 and Erk2 genes in mouse RPE.

166 f VU590 action by inhibition of native mouse RPE Kir7.1 current in patch-clamp experiment.

167 e expression of Kir7.1 channels in the mouse RPE.

168 wed photoreceptor degeneration, multilayered RPE, basal lamina deposits, and accumulations of monocyt

169 Multiple RPE fates in AMD, including intraretinal cells that are

170 We propose that mutant RPE Kir7.1 channels contribute directly to the abnormal

171 alescence was seen in 70.8% of eyes, and new RPE pigmentary changes developed in 56.2% of eyes.

172 then used to find that Muller glia, but not RPE cells, are essential for this process.

173 rocess we performed a microarray analysis of RPE cells pre- and post-FR treatment, and observed a mar

174 es and performed unbiased RNAseq analysis of RPE from Mertk (+/+) and Mertk (-/-) mice.

175 lly in a zone corresponding to the apices of RPE cells, at the roots of the RPE microvilli, and at th

176 1 mm(2), was larger than the initial area of RPE loss, 2.25 +/- 1.66 mm(2) (P < .01).

177 ts of the RPE microvilli, and at the base of RPE cells next to the Bruch's membrane.

178 din) was observed at the apices and bases of RPE cells.

179 te the potentially separate contributions of RPE valence (positive or negative) and surprise (absolut

180 ual function, and a rapid disorganization of RPE cells, ultimately leading to retinal degeneration.

181 (ADRD), and demonstrate that dysfunction of RPE cells alone is sufficient for the initiation of sub-

182 Dysregulation of RPE- and podocyte-derived VEGF is associated with neovas

183 We describe novel findings of RPE-BM thickness in normal individuals, a structure that

184 teristic RPE-tears, another atypical form of RPE-defect with overlying preserved photoreceptor layers

185 nterfering with the phagocytosis function of RPE associated with down-regulation of the expression of

186 nd lymphocytic responses to VZV infection of RPE cells, thereby providing a useful platform for futur

187 nsive body of literature on the influence of RPE on learning, little has been done to investigate the

188 Repair mechanisms such as ingrowth of RPE/drusenoid material and persistent subretinal fluid (

189 Over time, migration of RPE/drusenoid material right above the Bruch's membrane

190 (2)/year, was similar to the average rate of RPE loss, 0.33 +/- 0.38 mm(2)/year.

191 ), and MEK/ERK pathways in the regulation of RPE phagocytosis, confirmed by immunoblot analyses and i

192 largely distinct spatial representations of RPE valence and surprise.

193 Treatment of RPE cells with AnxA8 siRNA recapitulated exposure to FR,

194 and a critical component of the viability of RPE and photoreceptor cells.

195 The neural and emotional impact of RPEs is intact in major depression.

196 sis that depression attenuates the impact of RPEs.

197 t abolish the inhibitory effects of AICAR on RPE CFB expression.

198 However, their effect on RPE cells has not been fully elucidated.

199 though there was no main effect of stress on RPE.

200 t attributable to geographic atrophy (GA) or RPE-tears with overlying preserved photoreceptor layers.

201 ibe the distinctive features from pathologic RPE detachments and choroidal neovascularizations (CNVs)

202 ere the features distinctive from pathologic RPE detachments and CNVs.

203 they should be distinguished from pathologic RPE detachments and CNVs.

204 ot associated with significant peripapillary RPE displacement, OCD, or ONH tilt.

205 d phosphoproteomic analysis of phagocytosing RPE cells, utilizing three different experimental models

206 y continue to form a preserved photoreceptor-RPE complex that provides essential nutrients to the pho

207 RPE cells were differentiated into polarized RPE monolayers on permeable supports.

208 Primary cultures of porcine RPE cells were differentiated into polarized RPE monolay

209 CFB expression in ARPE-19 and human primary RPE cells in a dose-dependent fashion.

210 e cell line ARPE-19, cultured murine primary RPE cells, and RPE samples from live mice.

211 Three patients had a prior RPE-rip and were excluded.

212 lta-T-cell-deficient mice developed profound RPE and retinal damage at doses that caused minimal effe

213 horoidal reflectivity-vitreous reflectivity)/RPE reflectivity.

214 ostasis in the retina following AMD-relevant RPE injury and provide a foundation for understanding an

215 ry pathway: ECs secrete factors that remodel RPE basement membrane, and integrin receptors sense thes

216 ome critical region 8 (Dgcr8), thus removing RPE miRNA regulatory activity in mice by disrupting two

217 m, a dopamine target area known to represent RPEs.

218 or degeneration, and (4) absence of scrolled RPE or other signs of an RPE tear.

219 bnormally thin ONL co-localizing with severe RPE depigmentation and choroidal thinning.

220 nhibited proliferation and EMT of stimulated RPE cells by down-regulating Wnt (beta-catenin, LEF1) an

221 e associated with decreased ventral striatal RPE signaling during reinforcement learning (session 2),

222 ntify a novel link between IL-6 and striatal RPEs during reinforcement learning in the context of acu

223 proliferation (18% vs 10%; p=0.009) and sub-RPE fluid (65% vs 47%; p<0.001).

224 influences accumulation of this lipid in sub-RPE deposits remains elusive.

225 lone is sufficient for the initiation of sub-RPE lipoproteinaceous deposit (drusen) formation and ext

226 file, without any evidence of pathologic sub-RPE material.

227 Consistent with clinical studies, sub-RPE basal deposits were present beneath both control (un

228 at the ARMS2/HTRA1 locus with subretinal/sub-RPE hemorrhage and poorer visual acuity and of SNPs at t

229 sorganization and thinning of the submacular RPE on OCT when compared with normal controls.

230 ire lifespan of an organism, we believe that RPE-choroid preparation may represent a new and unique t

231 Here we demonstrate that RPE degeneration in human-cell-culture and mouse models

232 Overall, our results indicate that RPE cells carrying the m.3243A > G mutation have a reduc

233 It is possible that RPE may continue to form a preserved photoreceptor-RPE c

234 gression with age stratification showed that RPE thinning became apparent after age 45.

235 The RPE band appeared intact in all eyes.

236 The RPE was involved only mildly and transiently.

237 The RPE, like the liver, expresses enzymes required for fatt

238 nique biology of maculopathies affecting the RPE-ECM interface.

239 Hypertransmission of light below the RPE-basal lamina band correlated with dissociated RPE.

240 receptor matrix at the interface between the RPE and photoreceptor outer segments.

241 the absence of abnormal material between the RPE and the Bruch membrane were the features distinctive

242 eing the interdigitation zone or between the RPE and the Bruch's membrane.

243 etinal pigmented epithelium (RPE) death; the RPE also exhibits DICER1 deficiency, resultant accumulat

244 ce of a large choroidal vessel elevating the RPE and the absence of abnormal material between the RPE

245 ction of TSPO in cholesterol efflux from the RPE cells.

246 activation of Nf2 expression by Mitf in the RPE and suppression by Sox2 in retinal progenitor cells

247 ted that early stages of phagocytosis in the RPE are mainly characterized by pronounced changes in th

248 ry mechanisms underlying phagocytosis in the RPE are not fully understood, although dysfunction of th

249 ecific deletion of TGF-beta signaling in the RPE caused no obvious changes, specific deletion in vasc

250 essing and subsequent gene regulation in the RPE due to DICER1 deficiency also contributes to RPE cel

251 n-beta, and cGAS levels were elevated in the RPE in human eyes with geographic atrophy.

252 he same BMP lipids were also detected in the RPE of healthy human retina.

253 mice by increasing expression of CRRY in the RPE using a gene therapy approach.

254 leach and 5-fold lower retinyl esters in the RPE.

255 onded to large choroidal vessels lifting the RPE.

256 was analyzed to assess abnormalities of the RPE and choroid.

257 are key to supporting the metabolism of the RPE and preventing the accumulation of lipids that lead

258 defects in the survival and function of the RPE and retina.

259 ve the Bruch membrane within the dome of the RPE detachment, the choroidal stalks were all in the cho

260 the apices of RPE cells, at the roots of the RPE microvilli, and at the base of RPE cells next to the

261 ) a zone of attenuation or disruption of the RPE of at least 250 mum in diameter, (3) evidence of ove

262 rticipants with the respective change of the RPE signal in the nucleus accumbens.

263 help preserve the phagocytic function of the RPE while also exhibiting anti-inflammatory properties.

264 of mitochondria at the basal portion of the RPE, as identified by cytochrome C immunoreactivity, and

265 ctive foci was preceded by thickening of the RPE-basal lamina band.

266 both phase advances and phase delays of the RPE-choroid clock, thus suggesting that - as in other ti

267 An enlargement of the RPE-defect was apparent in the remaining 3 cases.

268 47 +/- 38 months after the occurrence of the RPE-defect were included (age range 71-87 years).

269 compromise the integrity and function of the RPE.

270 he cone phagosomes located in the top of the RPE.

271 gocytosis, one of the major functions of the RPE.

272 erapy suggests that complement attack on the RPE is an important etiologic factor in STGD1.

273 increased complement activation seen on the RPE of STGD1 mice.

274 Since the RPE cells persist for the entire lifespan of an organism

275 ALBP, cytochrome C, and GNB3 showed that the RPE interdigitations extend along the entire external se

276 based delivery systems were non-toxic to the RPE cells, chemically stable in porcine vitreous and del

277 rototypes (hydrophobic & hydrophilic) to the RPE cells.

278 enous microglia from the inner retina to the RPE layer, followed by (2) subsequent monocyte infiltrat

279 and between bands 3 and 4 corresponds to the RPE nuclei and melanosomes zone.

280 ll-trans-ROL movement from the retina to the RPE or may regulate all-trans-ROL storage within the RPE

281 ategy for intracellular drug delivery to the RPE targets but might also be useful in utilizing the RP

282 of all-trans-ROL from photoreceptors to the RPE.

283 t regeneration and retinal attachment to the RPE.

284 ts but might also be useful in utilizing the RPE cells as mediators of drug delivery to intracellular

285 ex-vivo isolated mouse retina ERG where the RPE is not attached to the isolated retina preparation.

286 normalized choroidal reflectivity, with the RPE as the bright reference standard and the vitreous as

287 lth of cones and their relationship with the RPE, and could help to form a better understanding of re

288 fragments of cone outer segments within the RPE led us to characterize the third band as the cone ph

289 ay regulate all-trans-ROL storage within the RPE.

290 yes with drusen exhibited a slightly thicker RPE compared with control eyes (+3.4 mum, P=0.012).

291 due to DICER1 deficiency also contributes to RPE cell death.

292 lective foci as seen on SD OCT correlated to RPE cells on histologic examination.

293 To determine why MerTK is critical to RPE function, we examined visual cycle intermediates and

294 We found that myeloid cell responses to RPE injury occur in stages: (1) an early mobilization of

295 tion, the nature of immune cell responses to RPE injury remains undefined.

296 TSPO-/- RPE cells also had significantly increased production of

297 nd HC-HA/PTX3 were not toxic to unstimulated RPE cells.

298 For central GA, the factors (P < 0.001) were RPE drusen complex abnormal thinning volume, intraretina

299 Ex vivo coculture of gammadelta T cells with RPE explants activated the production of anti-inflammato

300 related atrophy was more common in eyes with RPE humps (60.6% vs 34.4%; P < .05).