ライフサイエンスコーパス: apoptotic cell

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

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

3 idylserine (PtdSer) receptors that recognize apoptotic cells.

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

5 nding factors to promote the phagocytosis of apoptotic cells.

6 of eliciting anti-inflammatory responses to apoptotic cells.

7 osphatidylserine expressed on the surface of apoptotic cells.

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

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

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

11 ng chromatin in microparticles released from apoptotic cells.

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

13 e cell surface expression of calreticulin on apoptotic cells.

14 morphological changes like the extrusion of apoptotic cells.

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

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

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

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

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

20 ound to peripheral cellular regions in early apoptotic cells.

21 gocytes are highly specialized for engulfing apoptotic cells.

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

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

24 of macrophages following the phagocytosis of apoptotic cells.

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

26 hanistically, Tim-1 on Bregs is required for apoptotic cell (AC) binding to Bregs and for AC-induced

27 Apoptotic cell (AC) clearance (efferocytosis) is an evol

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

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

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

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

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

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

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

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

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

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

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

39 and Dock180 overexpression reduced the total apoptotic cell and apoptotic EC number and promoted the

40 tin ring (EAAR) that is assembled within the apoptotic cell and drives epithelial extrusion.

41 estrated morphological rearrangements of the apoptotic cell and its neighbors.

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

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

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

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

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

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

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

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

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

51 earance of extracellular particles including apoptotic cells and pathogens.

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

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

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

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

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

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

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

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

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

61 vocation of inflammatory T-cell responses to apoptotic cell antigens and failure of long-tolerance in

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

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

64 Although apoptotic cells are cleared quickly in almost all other

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

66 Apoptotic cells are typically disposed of without activa

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

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

69 hat is associated with increased circulating apoptotic cell autoantigens (AC-Ags) as well as increase

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

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

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

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

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

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

76 Phagocytosis of apoptotic cells by macrophages and spent photoreceptor o

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

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

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

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

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

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

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

84 Detection of apoptotic cells can therefore spatially compartmentalize

85 In apoptotic cells, caspase-initiated signaling cascades le

86 In vivo, apoptotic cell challenge drove a rapid, GCN2-dependent s

87 We have previously reported that apoptotic cell clearance activity or efferocytosis is co

88 g Megf10 with EMARDD mutations have impaired apoptotic cell clearance and impaired binding to C1q.

89 Efficient apoptotic cell clearance and induction of immunologic to

90 define a novel Megf10-dependent pathway for apoptotic cell clearance and show that Megf10 is a recep

91 We discuss how networks regulating apoptotic cell clearance are integrated to enable a rapi

92 chanism is neutrophil apoptosis, followed by apoptotic cell clearance by phagocytes such as macrophag

93 Previously, defects in apoptotic cell clearance have been linked to neurodegene

94 We examined the cause of impaired apoptotic cell clearance in human and murine lupus.

95 for the distal fragment, allowing conserved apoptotic cell clearance molecules to function in re-est

96 How the apoptotic cell clearance process is linked to macrophage

97 in Draper-I (a member of the CED-1 family of apoptotic cell clearance receptors) and a downstream kin

98 induction of anti-inflammatory responses by apoptotic cell clearance seems to dampen atherosclerosis

99 ampen atherosclerosis, because inhibition of apoptotic cell clearance worsens atherosclerosis.

100 mbined with the necessarily prompt nature of apoptotic cell clearance, makes it difficult to study th

101 idized low-density lipoprotein and promoting apoptotic cell clearance.

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

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

104 The removal of apoptotic cell corpses is important for maintaining home

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

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

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

108 spondin-1 type I repeats (3TSR) induced more apoptotic cell death (36.5 +/- 9.6%) in vitro compared t

109 cle arrest - and, in the absence of p53, non-apoptotic cell death - redundantly limit growth in ATR-d

110 ine the mechanisms by which phagocytes sense apoptotic cell death and discuss how phagocytosis is int

111 -inspired nanovesicle can efficiently induce apoptotic cell death and significantly inhibit tumor gro

112 Our findings showed that PL induced apoptotic cell death and suppressed the DNA binding acti

113 tituents, ultimately leading to induction of apoptotic cell death and the pathogenesis of various dis

114 he stress sensor, and protects cells against apoptotic cell death at both cellular and whole animal l

115 he IP3 R has been proposed to play a role in apoptotic cell death by uncoupling regions important for

116 eath is not limited to this natural turnover-apoptotic cell death can be induced by infection, inflam

117 decreases during necrotic, necroptotic, and apoptotic cell death caused by demyelinating, ischemic,

118 Transient activation of apoptotic cell death during early age correlated well wi

119 nd squirrel tubular cells are protected from apoptotic cell death during IBA.

120 ed tumor cells to CQ, resulting in increased apoptotic cell death following treatment.

121 Although the molecular effectors of apoptotic cell death have been largely annotated over th

122 e NF-kappaB pathway in HeLa cells and induce apoptotic cell death in both HeLa and Kym-1 cells.

123 5 was shown to be more effective in inducing apoptotic cell death in cancer cells as compared to norm

124 nstitutively activates caspase-8 and induces apoptotic cell death in human lung epithelial cells.

125 that combined checkpoint inhibition induces apoptotic cell death in KRAS- or BRAF-mutant tumor cells

126 ith the anti-HSF1 compounds strongly induced apoptotic cell death in MM cells.

127 tion, inhibited proliferation, and triggered apoptotic cell death in primary neonatal pig GMCs.

128 wn of FAIM2 expression increases Fas-induced apoptotic cell death in SCLC cells.

129 ic potential, anoikis resistance and induced apoptotic cell death in therapy-resistant EOC cells.

130 tor of cyclin-dependent kinase CDK7, induces apoptotic cell death in triple-negative breast cancers.

131 cAMP/PKA-Calpha and PKA-R1alpha/Bim mediate apoptotic cell death in WT S49 cells, kin(-) cells resis

132 Apoptotic cell death is important for the normal develop

133 n synthesis of MCL1, which, in turn, induces apoptotic cell death of cancer cells.

134 properties of molecules of the mitochondrial apoptotic cell death pathway.

135 at Galphaq/PKCzeta complexes link Galphaq to apoptotic cell death pathways.

136 ath (LCD) is a morphologically conserved non-apoptotic cell death process operating in Caenorhabditis

137 occurring to the NE, during the necrotic and apoptotic cell death process, using the xCELLigence syst

138 t, they become subject to elimination via an apoptotic cell death program known as anoikis.

139 block human B-cell proliferation and promote apoptotic cell death selectively in antibody-secreting B

140 a required step in the induction of type II apoptotic cell death that involves calcium mobilization

141 TcdA intoxication results in an apoptotic cell death that is dependent on the glucosyltr

142 opic expression of the Kv1.5 channel induces apoptotic cell death under conditions of hypoxia.

143 eld duodenum, there was a trend for elevated apoptotic cell death under most irradiation conditions;

144 dence on this transcriptional CDK and suffer apoptotic cell death upon CDK7 inhibition.

145 cumulation of ZnPc in MCF-7 cells, improving apoptotic cell death upon irradiation.

146 Simvastatin induced apoptotic cell death via the intrinsic apoptotic pathway

147 se activation or ultrastructural features of apoptotic cell death were observed.

148 Caspase-8 is a key initiator of apoptotic cell death where it functions as the apical pr

149 ssion in mouse MIN6 insulinoma cells induced apoptotic cell death with an increase in Bax activation

150 cells exhibited increased susceptibility and apoptotic cell death with oxidative stress.

151 CX-5461 (ie, the induction of p53-dependent apoptotic cell death), the inhibition of Pol I transcrip

152 believed to die through caspase 8-dependent apoptotic cell death, and chemotherapy is thought to pro

153 ers Bax and Bak are known to be resistant to apoptotic cell death, and previous we have shown that th

154 The process of apoptotic cell death, as defined at the molecular level,

155 ion of G4C2 repeats of varying length caused apoptotic cell death, but failed to generate DPRs.

156 Ferroptosis is an iron-dependent form of non-apoptotic cell death, but its molecular mechanism remain

157 an upstream regulator of a novel form of non-apoptotic cell death, called ferroptosis, whereas the mi

158 TAZ depletion in HeLa and D645 cells caused apoptotic cell death, we propose that isoform-specific Y

159 age, culminating in activity-dependent, non-apoptotic cell death.

160 roptosis, parthanatos, or other forms of non-apoptotic cell death.

161 y tissue abnormalities, such as necrosis and apoptotic cell death.

162 one of the most fundamental processes during apoptotic cell death.

163 als that cause mitochondrial dysfunction and apoptotic cell death.

164 ple tumor suppressive pathways, particularly apoptotic cell death.

165 age of lysosomal contents that culminates in apoptotic cell death.

166 activation, and mitotic catastrophe-induced apoptotic cell death.

167 CN cell proliferation and inducing intrinsic apoptotic cell death.

168 tion of the p38 MAPK pathway associated with apoptotic cell death.

169 eased proliferation but was due to decreased apoptotic cell death.

170 steryl ester load without causing detectable apoptotic cell death.

171 reast cancer cells to doxorubicin leading to apoptotic cell death.

172 ium, mitochondrial depolarization, and necro-apoptotic cell death.

173 for sensitizing TNBC to chemotherapy-induced apoptotic cell death.

174 to ABT-263 and ABT-199, which induced rapid apoptotic cell death.

175 with Abeta resulted in mitochondria-mediated apoptotic cell death.

176 ects mitochondria dynamics and protects from apoptotic cell death.

177 endent manner, followed by caspase-dependent apoptotic cell death.

178 smic reticulum to the mitochondria result in apoptotic cell death.

179 is an iron-dependent, oxidative form of non-apoptotic cell death.

180 ells exposed to KA or NMDA appear to undergo apoptotic cell death.

181 ough induction of G2/M cell cycle arrest and apoptotic cell death.

182 spase and plays a central role in activating apoptotic cell death.

183 to induce severe aneuploidy and, ultimately, apoptotic cell death.

184 tubular epithelial cells to progress towards apoptotic cell death.

185 deficiency increases cIAP1 stability during apoptotic cell death.

186 tion, and loss of TAX1BP1 is associated with apoptotic cell death.

187 rtant ramifications in diseases that involve apoptotic cell death.

188 al number of donor cells are lost because of apoptotic cell death.

189 rescue, we observe a significant increase in apoptotic cell density in Foxg1(-/-);Wnt8b(-/-) double m

190 ase of self antigens and danger signals from apoptotic cell-derived constituents that can result in i

191 uniquely programmed to process internalized apoptotic cell-derived fatty acids, cholesterol and nucl

192 y DFNA5 as a central molecule that regulates apoptotic cell disassembly and progression to secondary

193 sion of IDO1 in MPhis significantly enhanced apoptotic cell-driven IL-10 and suppressed IL-12 product

194 ffector of IDO1; thus, we tested its role in apoptotic cell-driven immune suppression.

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

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

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

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

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

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

201 Here we show that apoptotic cell extrusion is provoked by singularities in

202 ntractility at adherens junctions influences apoptotic cell extrusion.

203 of these results, we propose a mechanism for apoptotic cell extrusion: spontaneously formed topologic

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

205 Extrusion of apoptotic cells from epithelial tissues requires orchest

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

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

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

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

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

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

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

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

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

215 17.5 +/- 1.73 and a significant increase in apoptotic cells in islets.

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

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

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

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

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

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

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

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

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

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

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

227 . (2016) describe how "find-me" signals from apoptotic cells induce erythropoietin signaling within m

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

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

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

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

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

233 Moreover, this apoptotic cell-initiated pathway functioned independentl

234 on of surface molecules required for NKT and apoptotic cell interactions and developed suppressive im

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

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

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

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

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

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

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

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

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

244 Apoptotic cells, necrotic cores, and proinflammatory VCA

245 on, there is a positive relationship between apoptotic cell numbers and fluorescence intensities.

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

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

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

249 in are impaired in their abilities to induce apoptotic cell phagocytosis by murine peritoneal macroph

250 ing of old and new phagocyte functions after apoptotic cell phagocytosis demonstrates the enormity of

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

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

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

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

255 Some studies have linked apoptotic cell receptors on cardiac macrophages to tissu

256 ted from reduced microglial surveillance and apoptotic cell recognition receptor expression and was n

257 ve found that dendritic cells expressing the apoptotic cell-recognizing receptor CD300f play a crucia

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

259 in the dying cell to promote the increase in apoptotic cell refractility.

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

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

262 t CLL BCRs have the potential to internalize apoptotic cell RNA- or DNA-containing fragments with res

263 rovide new insights into the consequences of apoptotic cell sampling, advance our understanding of ho

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

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

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

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

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

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

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

271 on Env-CD4-coreceptor complexes triggers non-apoptotic cell surface exposure of the membrane lipid ph

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

273 that contractile stress transmitted from the apoptotic cell through E-cadherin adhesions elicits a me

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

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

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

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

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

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

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

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

282 Apoptotic cells undergo a series of morphological change

283 Impaired apoptotic cell uptake by MPhi also was seen in mice trea

284 and show that CD300f-dependent regulation of apoptotic cell uptake is essential for suppressing overa

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

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

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

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

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

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

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

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

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

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

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

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

297 Apoptotic cells were observed in the center of the first

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

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

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