ライフサイエンスコーパス: apoptotic cells

1 ote the shrinkage, death, and degradation of apoptotic cells.

2 h high affinity to C1q, an eat-me signal for apoptotic cells.

3 ity is later restored by active extrusion of apoptotic cells.

4 ns and play a major role in the clearance of apoptotic cells.

5 hatidylserine, an 'eat-me' signal exposed by apoptotic cells.

6 ound to peripheral cellular regions in early apoptotic cells.

7 st both foreign invaders and its own damaged/apoptotic cells.

8 ein S, which recognize phosphatidylserine on apoptotic cells.

9 ivation and DNA laddering pattern typical of apoptotic cells.

10 cterized by a deficiency in the clearance of apoptotic cells.

11 horylated Smad2/3, alphavbeta6 integrin, and apoptotic cells.

12 o internalize PtdSer-bearing targets such as apoptotic cells.

13 regulation of inflammation, and clearance of apoptotic cells.

14 ibition led to dysregulated fragmentation of apoptotic cells.

15 o bind to endogenous CERTL on the surface of apoptotic cells.

16 ate immunity, especially in the clearance of apoptotic cells.

17 erial infections and to promote clearance of apoptotic cells.

18 r matrix molecules, bacterial pathogens, and apoptotic cells.

19 utilized by live cells to remove neighboring apoptotic cells.

20 f tissue regrowth stimulated by signals from apoptotic cells.

21 ceramide, in accord with a previous study of apoptotic cells.

22 nding receptor, mediates the phagocytosis of apoptotic cells.

23 s, lower MCF-7/ADR cell viability and higher apoptotic cells.

24 signal phosphatidylserine on the surface of apoptotic cells.

25 e of pathogens, altered self-structures, and apoptotic cells.

26 beta3 is required for proper phagocytosis of apoptotic cells.

27 ity and the induction of immune tolerance by apoptotic cells.

28 is and clearance as well as efferocytosis of apoptotic cells.

29 utant retina contains an excessive number of apoptotic cells.

30 embrane and regulate uptake of C1q-opsonised apoptotic cells.

31 staining was used for the identification of apoptotic cells.

32 y understood how PS exposure is activated in apoptotic cells.

33 different lupus Ags including B cell Ags and apoptotic cells.

34 serine to trigger blood coagulation and mark apoptotic cells.

35 in, FBP1 may translocate to the cytoplasm in apoptotic cells.

36 long-lasting ectopic masses rarely contained apoptotic cells.

37 gocytes are highly specialized for engulfing apoptotic cells.

38 an "immunologically silent" clearance of the apoptotic cells.

39 ignals not to respond to the nucleic acid of apoptotic cells.

40 of macrophages following the phagocytosis of apoptotic cells.

41 ble for the silent uptake of vast numbers of apoptotic cells.

42 their dominant role in clearing the bulk of apoptotic cells.

43 city, high specificity, and high affinity to apoptotic cells.

44 idylserine (PtdSer) receptors that recognize apoptotic cells.

45 accine loaded with autologous HIV-1-infected apoptotic cells.

46 robe was fabricated to have high affinity to apoptotic cells.

47 nding factors to promote the phagocytosis of apoptotic cells.

48 of eliciting anti-inflammatory responses to apoptotic cells.

49 osphatidylserine expressed on the surface of apoptotic cells.

50 ze the 'eat-me' signal phosphatidylserine on apoptotic cells.

51 NA damage response (DDR) at telomeres in non-apoptotic cells.

52 ng chromatin in microparticles released from apoptotic cells.

53 terfere with the immune-silencing effects of apoptotic cells.

54 e cell surface expression of calreticulin on apoptotic cells.

55 morphological changes like the extrusion of apoptotic cells.

56 ase-mediated dUTP nick end labeling-positive apoptotic cells (8.3% +/- 1.4%) versus Ad-GFP control (4

57 c cells that participate in the clearance of apoptotic cells, a process known as efferocytosis.

58 Efficient clearance of apoptotic cells (AC) is pivotal in preventing autoimmuni

59 ly lower phagocytosis rate of early and late apoptotic cells accompanied by a reduced Mer tyrosine ki

60 Uptake of apoptotic cells (ACs) ("efferocytosis") by alveolar macr

61 aling maintains immune tolerance by clearing apoptotic cells (ACs) and inducing immunoregulatory sign

62 in turn, opsonize phosphatidylserine (PS) on apoptotic cells (ACs) and serve as bridging molecules be

63 Uptake of apoptotic cells (ACs) by macrophages ensures the nonimmu

64 oid dendritic cells inhibit the clearance of apoptotic cells (ACs) by marginal zone macrophages.

65 Clearance of apoptotic cells (ACs) by phagocytes (efferocytosis) prev

66 Although apoptotic cells (ACs) contain nucleic acids that can be

67 by dendritic cells processing material from apoptotic cells (ACs) in the steady-state.

68 Phagocytosis of apoptotic cells (ACs) is usually a potent immunoregulato

69 tosus (SLE), many self-antigens are found in apoptotic cells (ACs), and defects in removal of ACs fro

70 The phagocytosis of apoptotic cells (ACs), or efferocytosis, by DCs is criti

71 on phagocytes facilitates their clearance of apoptotic cells (ACs).

72 ish Health demonstrated that phagocytosis of apoptotic cells actively suppresses inflammation by inhi

73 activator receptor (uPAR) on the surface of apoptotic cells also had equally important inhibitory ef

74 or in control fish with gill disease without apoptotic cells, although transmission remains to be dem

75 They engulf bacteria and apoptotic cells and are better phagocytes than bone marr

76 The phagocytosis of apoptotic cells and associated vesicles (efferocytosis)

77 acCED-8, that promotes PS externalization in apoptotic cells and can induce ectopic PS exposure in li

78 ssue repair, wound healing, and clearance of apoptotic cells and cellular debris.

79 icobasal actomyosin cable that characterizes apoptotic cells and contributes force(s) for cell sheet

80 sine kinases promote phagocytic clearance of apoptotic cells and downregulate immune responses initia

81 urther contained less proliferating and more apoptotic cells and exhibited lower numbers of infiltrat

82 At baseline, the number of apoptotic cells and expression of total apoptosis-induci

83 nases that mediate activation of PKCdelta in apoptotic cells and have explored the use of tyrosine ki

84 ogether with immunohistochemical evidence of apoptotic cells and IL-15-producing cells proximal to B-

85 tein MFG-E8 mediates phagocytic clearance of apoptotic cells and influences the pathogenesis and prog

86 r by mutagenesis blocks vesicle formation in apoptotic cells and inhibits CPS, thus uncoupling apopto

87 s phosphatidylserine, the 'eat-me' signal on apoptotic cells and integrins alphavbeta3/alphavbeta5 in

88 rophages plays a pivotal role in eliminating apoptotic cells and invading pathogens.

89 cle cells in mice, TNF-alpha is expressed in apoptotic cells and is required for normal cell death.

90 ls in regulating the tolerogenic response to apoptotic cells and limiting autoimmunity.

91 wound closure and decreased accumulation of apoptotic cells and macrophages in the wounds.

92 ar interaction at intercellular junctions of apoptotic cells and macrophages, unlike other typical sc

93 ation through their role in the clearance of apoptotic cells and necrotic debris.

94 of macrophage CD36, a recognized receptor of apoptotic cells and oxidized lipids, in two models of ki

95 (such as epithelial cells) clear billions of apoptotic cells and particles on a daily basis.

96 earance of extracellular particles including apoptotic cells and pathogens.

97 ssion is required for efficient clearance of apoptotic cells and phagosome maturation.

98 flow cytometry; annexin-V status identified apoptotic cells and phosphorylation of intracellular kin

99 ABCF1 was released from apoptotic cells and selectively bound to shed POS vesicl

100 lasma membrane, is exposed on the surface of apoptotic cells and serves as an 'eat-me' signal to trig

101 Blood-derived monocytes remove apoptotic cells and terminate inflammation in settings a

102 t, we examine the role of IDO in response to apoptotic cells and the impact of IDO on Treg cell funct

103 o implement assays regarding cTK function in apoptotic cells and the in vivo imaging varies depending

104 ines the correlation between the presence of apoptotic cells and their effect on fibroblast phenotype

105 The nature of signaling between apoptotic cells and their neighboring cells remains larg

106 led in situ were imaged successfully in both apoptotic cells and tumour tissues using three-dimension

107 UV- or human immunodeficiency virus-induced apoptotic cells and with complement enhance the phagocyt

108 Eiger is produced in apoptotic cells and, through activation of the c-Jun N-t

109 osomes increased efferocytosis (clearance of apoptotic cells) and gene expression associated with alt

110 ve macrophage efferocytosis (phagocytosis of apoptotic cells) and resolution, but little is known reg

111 h increased survival and a reduced number of apoptotic cells, and adult male offspring exhibited high

112 pendent on the HP, whereas anti-nuclear Abs, apoptotic cells, and dsDNA binding are HP independent an

113 epithelial cells, mediating phagocytosis of apoptotic cells, and it may also act as a costimulatory

114 nstrate that PE is exposed on the surface of apoptotic cells, and promotes their phagocytic uptake by

115 loping chick limb buds control the number of apoptotic cells, and that MafB/cJun heterodimers lead to

116 AI1), which recognizes phosphatidylserine on apoptotic cells, and the intracellular signaling interme

117 innate immune response, the phagocytosis of apoptotic cells, and the restoration of vascular integri

118 ML) of pathogens, as well as of malignant or apoptotic cells, and thus constitutes an integral part o

119 ed significant (P </=0.01) increase of early apoptotic cells (annexin V positive) and late apoptosis

120 Apoptotic cells are a source of autoantigens and impairm

121 Although apoptotic cells are also known to suppress LPS-induced p

122 Apoptotic cells are capable of inducing tolerance by alt

123 Understanding the pathways by which apoptotic cells are cleared in the CNS is relevant to ma

124 Although apoptotic cells are cleared quickly in almost all other

125 en our understanding of the process by which apoptotic cells are cleared.

126 If apoptotic cells are not scavenged, they progress to a ly

127 Apoptotic cells are typically disposed of without activa

128 Collectively, these data identify apoptotic cells as a new type of cue that induces signal

129 over, the CD31(+)F4/80(+) cells phagocytosed apoptotic cells as functionally matured macrophages, adh

130 etains its ability to preferentially bind to apoptotic cells at a level comparable to the native prot

131 Defective in vivo clearance of apoptotic cells augmented in vivo accumulation of DAB4 i

132 phic chondrocytes revealed modest numbers of apoptotic cells but high levels of antiapoptotic Bcl-2 e

133 y of the defects induced for phagocytosis of apoptotic cells but not healthy cells suggests that cell

134 ong endogenous ligands, C1q binds to DNA and apoptotic cells, but whether C1q binds to nuclear DNA in

135 cerebellum and have impaired phagocytosis of apoptotic cells by astrocytes ex vivo We also report tha

136 We conclude that recognition of apoptotic cells by BAI1 contributes to their clearance i

137 Phagocytosis of apoptotic cells by both professional and semi-profession

138 fic 6 (GAS6), which mediates phagocytosis of apoptotic cells by bridging cells with surface exposed p

139 polyinosinic acid inhibited phagocytosis of apoptotic cells by CD138(+) MPhi.

140 Phagocytosis of apoptotic cells by macrophages and spent photoreceptor o

141 Successful efferocytosis of apoptotic cells by monocyte-derived macrophages resulted

142 The engulfment and subsequent degradation of apoptotic cells by phagocytes is an evolutionarily conse

143 The engulfment of apoptotic cells by phagocytes, a process referred to as

144 Efferocytosis, a process of clearance of apoptotic cells by phagocytes, is essential for successf

145 Recognition and removal of apoptotic cells by professional phagocytes, including de

146 its potent ability to stimulate clearance of apoptotic cells by skin fibroblasts.

147 cargo and that EMPs affect the clearance of apoptotic cells by specialized macrophages.

148 eal-time method to detect the recognition of apoptotic cells by viable adherent responder cells, usin

149 At an injury site, efficient clearance of apoptotic cells by wound macrophages or efferocytosis is

150 When nucleoli were isolated from non-apoptotic cells, C1q also bound to these structures.

151 However DNA, STING agonists, and apoptotic cells can also promote tolerogenic responses v

152 ing the past decade it has become clear that apoptotic cells can produce diverse signals that have a

153 Apoptotic cells can produce signals to instruct cells in

154 For example, apoptotic cells can release factors that influence the p

155 Detection of apoptotic cells can therefore spatially compartmentalize

156 In apoptotic cells, caspase-initiated signaling cascades le

157 its role in promoting PS externalization in apoptotic cells, ced-8 is important for cell corpse engu

158 opes (OSE), present on oxidized LDL (OxLDL), apoptotic cells, cell debris and modified proteins in th

159 Gipr(-/-betaCell) mice lowers the number of apoptotic cells compared to that seen in MIP-Cre control

160 howed greater ABCA1 induction in response to apoptotic cells compared with those from control animals

161 r measuring the cell uptake of PET tracer in apoptotic cells, correlating doxorubicin (Dox)-induced c

162 Macrophages clear millions of apoptotic cells daily and, during this process, take up

163 th their defect in the cross-presentation of apoptotic cells, DC-specific Vps34-deficient animals dev

164 Mechanistically, apoptotic cells did not directly fuse with the healthy m

165 E but is not required for reactivity against apoptotic cells, dsDNA, chromatin, anti-nuclear Abs, or

166 Moreover, PSR-1 enriches and clusters around apoptotic cells during apoptosis.

167 Clearance of apoptotic cells (efferocytosis) is achieved through phag

168 red ability of arterial phagocytes to uptake apoptotic cells (efferocytosis) promotes lesion growth a

169 to remove foreign materials, pathogens, and apoptotic cells efficiently.

170 himeras manifested increased accumulation of apoptotic cells, enhanced fibrotic area, and larger infa

171 d with hypoxia and signaling associated with apoptotic cells, especially between nonmetastatic breast

172 To this end, apoptotic cells express specific eat-me signals, such as

173 on of miR-200b mimic increased the number of apoptotic cells following 4-HNE treatment.

174 protective effects were observed, with fewer apoptotic cells found in the spinal cords of SIRT1-overe

175 xecuting a pivotal role in the scavenging of apoptotic cells from affected tissue.

176 Extrusion of apoptotic cells from epithelial tissues requires orchest

177 sis and found that LFG protects only type II apoptotic cells from FasL-induced death in a Bcl-XL depe

178 tricted to the peritoneum and may help clear apoptotic cells from tissues such as the lung, helping t

179 CNS, and that microglial phagocytosis of the apoptotic cells generated during adult neurogenesis is n

180 t target macrophages, endothelial cells, and apoptotic cells have also been tested in small groups of

181 hways modulated in phagocytes in response to apoptotic cells have been linked to chronic inflammatory

182 ll death, coupled with impaired clearance of apoptotic cells, have been implicated as causes of failu

183 o be induced by the successful engulfment of apoptotic cells, highlighting the importance of early ex

184 The clearance of apoptotic cells (i.e. efferocytosis) is a key modulator

185 DC ingestion of infected apoptotic cells (IACs) drive prostaglandin E2 (PGE2) sec

186 Genetic ablation of sensors of apoptotic cells impaired the proliferation of tissue-res

187 y also significantly increased the number of apoptotic cells in adipose tissue.

188 an increase in the number of early and late apoptotic cells in both the infected and bystander cell

189 17.5 +/- 1.73 and a significant increase in apoptotic cells in islets.

190 in the uptake of phosphatidylserine-exposing apoptotic cells in macrophages and dendritic cells.

191 exhibited reduced numbers of osteoblasts and apoptotic cells in periodontium and diminished expressio

192 granzyme B inhibitor decreased the number of apoptotic cells in the CL group, the use of z-VAD-FMK ha

193 rt that Megf10-deficient mice have increased apoptotic cells in the developing cerebellum and have im

194 ere associated with abnormal accumulation of apoptotic cells in the gut.

195 s of CD68(+) alveolar macrophages as well as apoptotic cells in the lungs after blockage.

196 tify a novel role for Megf10 in clearance of apoptotic cells in the mammalian developing brain with p

197 , mice lacking BAI1 had increased numbers of apoptotic cells in their aortic roots, which correlated

198 Here we focus on the homeostatic removal of apoptotic cells in tissues.

199 idylserine binding in vitro and clearance of apoptotic cells in vivo.

200 murine and human macrophage efferocytosis of apoptotic cells, independent of macrophage polarization

201 ified a novel mode of communication by which apoptotic cells induce additional apoptosis in the same

202 . (2016) describe how "find-me" signals from apoptotic cells induce erythropoietin signaling within m

203 Herein we report apoptotic cells induce expression of the chemokine CCL22

204 Our laboratory has reported that apoptotic cells induce tolerance by a mechanism dependen

205 fuse with the healthy myoblasts, rather the apoptotic cells induced a contact-dependent signalling w

206 ection of anti-PR3 ANCAs with PR3-expressing apoptotic cells induced a Th17 response, revealing a GPA

207 cells and inhibits the production of ROS and apoptotic cells induced by gentamicin.

208 Systemic challenge with apoptotic cells induced rapid production of CCL22 in CD1

209 sufficient, but IL-4 or IL-13 together with apoptotic cells induced the tissue repair program in mac

210 de-acetaldehyde-adducts), which are found on apoptotic cells, inflammatory tissues, and atherosclerot

211 y acting on phagocytes, notably macrophages, apoptotic cells inhibit immunological and inflammatory r

212 Exposing THP-1 cells to apoptotic cells inhibited IL-6 production from 1340 to <

213 inished the ability of macrophages to ingest apoptotic cells, interaction between vitronectin with ur

214 Disassembly of apoptotic cells into smaller fragments (a form of extrac

215 ction of proteolytic fragments released from apoptotic cells into the peripheral blood may serve as a

216 The removal of apoptotic cells is an innate function of tissue macropha

217 The clearance of apoptotic cells is critical for both tissue homeostasis

218 In ced-11 mutants, the degradation of apoptotic cells is delayed.

219 tissue physiology, and the prompt removal of apoptotic cells is equally essential to avoid the undesi

220 Tolerance to apoptotic cells is essential to prevent inflammatory pat

221 Defective clearance of apoptotic cells is frequently associated with perpetuati

222 Phagocytosis of apoptotic cells is thus coupled to specific functions, f

223 unction in host defense and the clearance of apoptotic cells, macrophages are now increasingly recogn

224 However, in addition to apoptotic cells, macrophages can engulf foreign bodies t

225 aling and that CD36-mediated phagocytosis of apoptotic cells may serve as an important pathway in the

226 ized by abundant BAFF-positive cells but few apoptotic cells (mostly B cells).

227 Following MFG-E8-mediated engulfment of apoptotic cells, myofibroblasts acquired antiinflammator

228 lop bile duct hyperplasia and show increased apoptotic cells, necrosis, regenerative nodules, and evi

229 increased lipid and macrophage accumulation, apoptotic cells, necrotic cores, and interleukin 1beta i

230 Apoptotic cells, necrotic cores, and proinflammatory VCA

231 During phagocytosis of apoptotic cells or in response to inflammation-associate

232 not affect CXCL1 expression or the number of apoptotic cells or infiltrating leukocytes.

233 of plaque necrosis is defective clearance of apoptotic cells, or efferocytosis, by lesional macrophag

234 classic T-independent Ag that is exposed on apoptotic cells, oxidized phospholipids, and bacterial p

235 Effective removal of apoptotic cells, particularly apoptotic neutrophils, is

236 rythematosus, where impaired phagocytosis of apoptotic cells plays a role in the pathogenesis of the

237 d selectively bound to shed POS vesicles and apoptotic cells, possibly via externalized phosphatidyls

238 Using a cell culture model, we show that apoptotic cells potently activate AMP-activated protein

239 dating the mechanisms by which the different apoptotic cells present during fibrotic wound healing af

240 Here we show that a fraction of apoptotic cells produce and release CrkI-containing micr

241 M-1-mediated epithelial cell phagocytosis of apoptotic cells protects the kidney after acute injury b

242 of such interactions of SCARF1 with C1q and apoptotic cells provides insight into the molecular mech

243 ic mice overexpressing BAI1, these had fewer apoptotic cells, reduced inflammation, and attenuated di

244 lls, but whether C1q binds to nuclear DNA in apoptotic cells remains to be investigated.

245 It was shown that clearance of apoptotic cells results in tolerance induction to cleare

246 higher levels of MerTK and, when exposed to apoptotic cells, secreted proreparative cytokines, inclu

247 e observed a large number of binucleated and apoptotic cells-signs of failed cytokinesis that we also

248 stimulated with autoantibody ICs containing apoptotic cells, small nuclear RNPs (snRNPs), or DNA, or

249 Mer and Axl exhibit a marked accumulation of apoptotic cells specifically in neurogenic regions of th

250 Higher numbers of apoptotic cells, stronger C4d and SAP deposition, and ex

251 ction and specificity of the cTK reporter in apoptotic cells, such as assays for measuring the cell u

252 a (CLL) BCRs interacts with Ags expressed on apoptotic cells, suggesting that CLL BCRs have the poten

253 und parameter changes from those of in vitro apoptotic cells, suggesting that these different methods

254 and integrin alphaV promote phagocytosis of apoptotic cells, support the concept that EBOV relies on

255 induced by self-antigens alone, we injected apoptotic cells that carry the same oxidation-specific e

256 lammatory granulocytes (Ly-6C(int)G(hi)) and apoptotic cells; the increased production of IFN-gamma a

257 lack of efficient SAP-mediated clearance of apoptotic cells through FcgammaRs.

258 controls signaling-mediated phagocytosis of apoptotic cells through its target, Death Domain1alpha (

259 for the maturation of phagosomes containing apoptotic cells, through recruitment of the Rab GTPase U

260 bridging molecule between the macrophage and apoptotic cells, thus executing a pivotal role in the sc

261 Many viruses mimic apoptotic cells, thus exploiting TAM receptors for attac

262 y and compensate for the increased number of apoptotic cells, thus maintaining phagocytosis and apopt

263 NX1) release nucleotide find-me signals from apoptotic cells to attract phagocytes.

264 brane-initiated pathway that is triggered by apoptotic cells to enhance ABCA1 within engulfing phagoc

265 means of conferring immunogenic tolerance to apoptotic cells to ensure silent, noninflammatory cell d

266 Dendritic cells carry apoptotic cells to lymph nodes where they signal the eme

267 process and present antigens associated with apoptotic cells to MHC class I-restricted T cells.

268 Apoptotic cells trigger immune tolerance in engulfing ph

269 ymatically active membrane-associated PR3 on apoptotic cells triggered secretion of inflammatory cyto

270 during engulfment, the lipid content of the apoptotic cells triggers the lipid-sensing receptor live

271 Calreticulin is detectable on the surface of apoptotic cells under some apoptosis-inducing conditions

272 Apoptotic cells undergo a series of morphological change

273 minimal handle for the efficient labeling of apoptotic cells using a fluorogenic tetrazine dye in a p

274 fferent doses, and the immunolabeling of the apoptotic cells using quantum dot reporters.

275 diate specific signals during recognition of apoptotic cells versus other ligands, and how this might

276 Additionally, exogenous calreticulin binds apoptotic cells via a higher-affinity calcium-dependent

277 timulation of LXR enhances the engulfment of apoptotic cells via regulating directly and indirectly t

278 nger receptor SCARF1 to recognize and engulf apoptotic cells via the complement component C1q.

279 By contrast, the recognition of apoptotic cells was dispensable for cytokine-dependent i

280 tion in fibrosis severity, a 56% increase in apoptotic cells was found without an increase in apoptot

281 Uptake of apoptotic cells was increased in lungs of mice that rece

282 Reduced macrophage clearance of apoptotic cells was mediated in part by H. pylori-induce

283 eir phagocytosis, such that uptake of larger apoptotic cells was reduced whereas engulfment of microv

284 isoform BAX-beta, exclusively transcribed in apoptotic cells, was negatively correlated.

285 e, (99m)Tc-labeled Duramycin, which binds to apoptotic cells, was used to measure pulmonary cell deat

286 failure leads to macrophage phagocytosis of apoptotic cells, we evaluated in vitro and in vivo wheth

287 TUNEL-positive apoptotic cells were dramatically decreased, and two apo

288 nificant lower viabilities and more necrotic/apoptotic cells were found when these cancer cells were

289 Apoptotic cells were more numerous in MAFIA versus clodr

290 In a recent study, apoptotic cells were newly identified as a type of cue t

291 Apoptotic cells were observed in the center of the first

292 ain edema, hematoma volume and the number of apoptotic cells were quantified.

293 liferative cells and decreased the number of apoptotic cells, which led to increased osteoblasts.

294 cells displayed hyperactive phagocytosis of apoptotic cells, which stimulated excessive TNF-alpha se

295 Binding was impaired 95% by pretreating apoptotic cells with annexin V, underscoring the require

296 Notably, preopsonization of the apoptotic cells with C3 activation fragments rectified t

297 devoid of proliferating cells and contained apoptotic cells with intense Edar transcripts and reduce

298 ulosis cases had a higher proportion of late apoptotic cells within the CD3(+)PD-1(+) subset.

299 macrophages in the CNS and higher numbers of apoptotic cells within the CNS parenchyma of LIGHT-defic

300 elated with the fraction of slow cycling and apoptotic cells within the four TPA subsets.