ライフサイエンスコーパス: efferocytosis

1 through a specialized form of phagocytosis (efferocytosis).

2 during the phagocytosis of apoptotic cells (efferocytosis).

3 impaired ability to ingest apoptotic cells (efferocytosis).

4 lfment by phagocytic cells (a process called efferocytosis).

5 vbeta3/alphavbeta5 in macrophages to trigger efferocytosis.

6 ivation and F-actin remodeling that promotes efferocytosis.

7 pendent manner when stimulated by MFG-E8 and efferocytosis.

8 D1 and D3 reduced inflammation by promoting efferocytosis.

9 es its dissemination in a host by exploiting efferocytosis.

10 are required at least for the initiation of efferocytosis.

11 ant but lesser roles in antigen sampling and efferocytosis.

12 K reversed the suppressive effect of 5-HT on efferocytosis.

13 rance of apoptotic cells, a process known as efferocytosis.

14 e lipid-laden necrotic core through impaired efferocytosis.

15 the 5-HT transporter prevented 5-HT-impaired efferocytosis.

16 mulated each other's expression and enhanced efferocytosis.

17 had equally important inhibitory effects on efferocytosis.

18 rdiomyocytes, and a reduced index of in vivo efferocytosis.

19 k between chronic inflammation and defective efferocytosis.

20 ly activated (M2) macrophages and neutrophil efferocytosis.

21 associated with impaired macrophage/monocyte efferocytosis.

22 uPAR or Abs to uPAR significantly diminished efferocytosis.

23 apoptotic cells by phagocytes is defined as efferocytosis.

24 icles contributed to SPM biosynthesis during efferocytosis.

25 idylinositol 3-phosphatase, is elevated upon efferocytosis.

26 on of C3 on apoptotic cells and C3-dependent efferocytosis.

27 lin-resistance syndrome may adversely affect efferocytosis.

28 eserving the viability of macrophages during efferocytosis.

29 ega-3 FAs contribute to decreased macrophage efferocytosis.

30 lls, a process that has recently been termed efferocytosis.

31 GB1 by PS eliminates the effects of HMGB1 on efferocytosis.

32 concentrations of HMGB1, inhibits neutrophil efferocytosis.

33 nvolvement of PAI-1 in modulating neutrophil efferocytosis.

34 osis, little is known about their effects on efferocytosis.

35 sought to determine whether statins enhanced efferocytosis.

36 apoptotic cancer cells in a process known as efferocytosis.

37 bca1, three proteins that promote macrophage efferocytosis.

38 nsibility of macrophages in a process called efferocytosis.

39 gnaling within macrophages to prime them for efferocytosis.

40 miR-126 attenuates HG-induced impairment of efferocytosis.

41 h specifically regulates and is regulated by efferocytosis.

42 phage cholesterol homeostasis with defective efferocytosis.

43 of DD1alpha, two proteins known to influence efferocytosis.

44 expansion of the necrotic core by impairing efferocytosis.

45 d we found no evidence of defective lesional efferocytosis.

46 as associated with significant inhibition of efferocytosis.

47 is signaling, and downstream consequences of efferocytosis.

48 d leads to macrophage death and insufficient efferocytosis.

49 gocytosis, phagolysosomal acidification, and efferocytosis.

50 y taken up by uninfected macrophages through efferocytosis, a dedicated apoptotic cell engulfment pro

51 Efferocytosis, a process of clearance of apoptotic cells

52 Diabetic db/db mice suffered from impaired efferocytosis accompanied with persistent inflammation a

53 We found that the abrogation of efferocytosis affected neither the ability of circulatin

54 limited inflammation and enhanced macrophage efferocytosis after sterile injury, when compared with A

55 tively active Rac1 overexpression rescued AM efferocytosis against the effects of ceramide.

56 njury, alternative macrophage activation and efferocytosis, alternate sources of fibroblasts, cellula

57 t than resolvin D1 in stimulating human MPhi efferocytosis, an action not shared by leukotriene B(4).

58 Cs demonstrated that PGE(2) generated during efferocytosis and acting via EP2 accounts for subsequent

59 ADAM17 deficiency leads to a 60% increase in efferocytosis and an enhanced anti-inflammatory phenotyp

60 binding protein 9 (RANBP9)--that mediates DC efferocytosis and antigen cross-presentation.

61 novel mechanism by which 5-HT might disrupt efferocytosis and contribute to the pathogenesis of auto

62 ge function related to reversal of defective efferocytosis and could be particularly important in typ

63 o Mtb infection and mediates the power of DC efferocytosis and cross-presentation.

64 In the setting of LPS-induced ALI, enhanced efferocytosis and decreased numbers of neutrophils were

65 The defect in efferocytosis and elevated apoptosis sensitivity of APOE

66 s better understand the relationship between efferocytosis and inflammation.

67 essed by phagocytic cells, where it promotes efferocytosis and inhibits inflammatory signaling.

68 MFG-E8) is a bridge protein that facilitates efferocytosis and is associated with suppression of proi

69 Mice lacking myeloid Drp1 showed defective efferocytosis and its pathologic consequences in the thy

70 ges, but the mechanisms underlying defective efferocytosis and its possible links to impaired resolut

71 lation using the inhibitor Stattic decreased efferocytosis and M2 macrophage polarization in vitro, w

72 deficient apoptotic bodies were resistant to efferocytosis and not efficiently cleared by neighboring

73 irmed the ability of Plg/Pla to both promote efferocytosis and override the prosurvival effect of LPS

74 ed the effects of MEKi on in vivo macrophage efferocytosis and polarization.

75 ceptor c-Mer tyrosine kinase (MerTK) reduces efferocytosis and promotes plaque necrosis and defective

76 Elevated macrophage miR-21 promotes efferocytosis and silences target genes PTEN and PDCD4,

77 nique model to examine relationships between efferocytosis and subsequent inflammation resolution, ti

78 m infarcted hearts altered their capacity of efferocytosis and subsequently blunted vascular endothel

79 ular basis by which these antibodies inhibit efferocytosis and ultimately lead to scar of the fetal c

80 phagocyte system being critical in mediating efferocytosis and wound debridement and bridging the gap

81 s in cell survival, clearance of dead cells (efferocytosis), and suppression of inflammation, which a

82 and monocyte migration, enhanced macrophage efferocytosis, and accelerated tissue regeneration in pl

83 ptor CD36 as a major contributor to enhanced efferocytosis, and CD36 surface levels are elevated on m

84 1, reversed the inhibitory effect of 5-HT on efferocytosis, and decreased cellular peritoneal inflamm

85 ns resolution intervals, enhances macrophage efferocytosis, and temporally regulates local levels of

86 altered macrophage programming and decreased efferocytosis, and that PPARgamma agonism would enhance

87 ative stress and necrosis, improved lesional efferocytosis, and thicker fibrous caps.

88 imulated neutrophil apoptosis and macrophage efferocytosis ( approximately 45%).

89 ese results support glucocorticoid-augmented efferocytosis as a potential explanation for the epidemi

90 accumulation was partially due to decreased efferocytosis as the ratio of free to cell-associated ap

91 Using a spleen efferocytosis assay and targeted genetic deletion in mic

92 MFG-E8(-/-) mice displayed impaired efferocytosis associated with exaggerated inflammatory r

93 Although many efferocytosis-associated receptors have been described i

94 tion of 5-HTR2a and 5-HTR2b had no effect on efferocytosis, but blockade of the 5-HT transporter prev

95 we uncover a key role for CCN1 in neutrophil efferocytosis by acting as a bridging molecule that bind

96 However, the regulation of efferocytosis by activation of TLRs has not been well ch

97 We investigated the relationship of efferocytosis by airway (induced sputum) macrophages and

98 Efferocytosis by airway macrophages was assessed in obes

99 We hypothesized that S. aureus impairs efferocytosis by alveolar macrophages (AMs) through the

100 resistant to proteolysis and suppression of efferocytosis by cleavage-inducing stimuli.

101 nti-human IL-10 receptor-alpha antibody, and efferocytosis by IL-10-deficient Mphis was markedly redu

102 tin appeared to exert its positive effect on efferocytosis by inhibiting RhoA, because it 1) decrease

103 Inhibition of efferocytosis by LPS was found to be positively associat

104 extent than Rac-1, and 2) prevented impaired efferocytosis by lysophosphatidic acid, a potent inducer

105 Here we demonstrate that efferocytosis by macrophages from CGD (gp91(phox)(-/-))

106 Efferocytosis by macrophages reflected PPARgamma activat

107 Efferocytosis by macrophages was 40% lower in obese than

108 natants, and F-actin staining; apoptosis and efferocytosis by morphology and flow cytometry; and GCS

109 5-HT impaired efferocytosis by murine peritoneal macrophages and human

110 venger receptors to drive recruitment of and efferocytosis by neutrophils.

111 mediates coordinated negative regulation of efferocytosis by resident murine and human tissue macrop

112 T1, which had not previously been linked to efferocytosis by tissue Mo.

113 ent Immunity papers provide new insight into efferocytosis by tissue-resident macrophages.

114 Uptake of apoptotic cells (ACs) ("efferocytosis") by alveolar macrophages (AMos) reduces t

115 e ingestion of apoptotic cells (ACs; termed "efferocytosis") by phagocytes has been shown to trigger

116 e clearance of apoptotic inflammatory cells (efferocytosis) by airway macrophages was associated with

117 A decreased clearance of apoptotic cells (efferocytosis) by alveolar macrophages (AM) may contribu

118 of apoptotic cells and associated vesicles (efferocytosis) by DCs is an important mechanism for both

119 matory cells and their subsequent clearance (efferocytosis) by macrophages (Mphis) are key mechanisms

120 recognition and removal of apoptotic cells (efferocytosis) by phagocytes are potently anti-inflammat

121 important for their recognition and removal (efferocytosis) by phagocytes, a requisite step for resol

122 he phagocytosis of apoptotic cells (ACs), or efferocytosis, by DCs is critical for self-tolerance and

123 s defective clearance of apoptotic cells, or efferocytosis, by lesional macrophages, but the mechanis

124 apoptosis and, if not efficiently cleared by efferocytosis, can undergo secondary necrosis, leading t

125 reased sensitivity to apoptosis and impaired efferocytosis capacity of TRAF6-deficient macrophages, r

126 Clodronate liposomes increased efferocytosis (clearance of apoptotic cells) and gene ex

127 mice are much more prone to apoptosis during efferocytosis compared to wild-type cells.

128 s isolated from APOE4 mice were defective in efferocytosis compared with APOE3 macrophages.

129 Based on these observations, we suggest that efferocytosis (corpse clearance) could contribute to pro

130 rstanding pathways that regulate and enhance efferocytosis could be harnessed to combat infection and

131 aberrant macrophage programming and impaired efferocytosis delay resolution of inflammation.

132 in wild-type macrophages reduced macrophage efferocytosis, demonstrating a central role for IL-4.

133 This process, termed efferocytosis, depends on cooperation between the phagoc

134 Defective efferocytosis drives important diseases, including ather

135 assess the causal significance of disrupting efferocytosis during myocardial infarction.

136 mice reduced macrophage CD206 expression and efferocytosis during peritonitis.

137 l role in the clearance of apoptotic cells - efferocytosis - during nematode development.

138 r targets to test how MerTK cleavage affects efferocytosis efficiency and inflammation resolution in

139 phages with apoptotic cancer cells increased efferocytosis, elevated MFG-E8 protein expression levels

140 tor (uPAR) as a "don't eat me" signal during efferocytosis, experiments addressed whether surface bou

141 h some of the engulfment ligands involved in efferocytosis have been identified and studied in vitro,

142 The mechanism of ceramide-induced efferocytosis impairment was dependent on generation of

143 bers and increasing neutrophil apoptosis and efferocytosis in a serine-protease inhibitor-sensitive m

144 There was also defective macrophage efferocytosis in atherosclerotic lesions of ob/ob;Ldlr(-

145 tor, and that increased MerTK expression and efferocytosis in CaMKIIgamma-deficient macrophages is de

146 inflammation, we hypothesized that impaired efferocytosis in CGD due to macrophage skewing contribut

147 ator in DC cross-presentation that increases efferocytosis in DCs and intrinsically enhances the capa

148 opsonization also increased phagocytosis and efferocytosis in macrophage foam cells.

149 However, the impact of efferocytosis in metastatic tumor growth is unknown.

150 s have evolutionarily conserved functions in efferocytosis in metazoans.

151 METHODS AND We quantified efferocytosis in peritoneal macrophages and in atheroscl

152 ed with a MerTK inhibitor exhibited impaired efferocytosis in postpartum tumors, a reduction of M2-li

153 ence, antiinflammatory programs activated by efferocytosis in the lung have the undesirable potential

154 Finally, lovastatin increased efferocytosis in the naive murine lung and ex vivo in ch

155 idermal growth factor 8 protein and enhanced efferocytosis in vitro and in situ.

156 These findings indicate that statins enhance efferocytosis in vitro and in vivo, and suggest that the

157 his study, we show that lovastatin increased efferocytosis in vitro in an 3-hydroxyl-3-methylglutaryl

158 R), which can inhibit thrombosis in mice and efferocytosis in vitro.

159 Importantly, enhanced efferocytosis in vivo by macrophages lacking ADAM17 is C

160 plex that mediates functionally important DC efferocytosis in vivo may have implications for future s

161 before intratracheal instillation decreased efferocytosis in vivo.

162 oid the pathologic consequences of defective efferocytosis in vivo.

163 In vivo comparison of macrophage efferocytosis in wild-type and Adam17-null hematopoietic

164 alternative (M2) programming associated with efferocytosis, including peroxisome proliferator-activat

165 Efferocytosis increased specialized pro-resolving mediat

166 M. tuberculosis is killed only after efferocytosis, indicating that apoptosis itself is not i

167 Therefore, efferocytosis-induced IL-4 production and activation of

168 We report that efferocytosis-induced miR-21, by silencing PTEN and GSK3

169 death during postpartum involution triggers efferocytosis-induced wound-healing cytokines in the tum

170 Whereas MerTK deficiency promotes defective efferocytosis, inflammation, and plaque necrosis in adva

171 hat the inhibitory effects of vitronectin on efferocytosis involve interactions with both the engulfi

172 is a summary of recent data indicating that efferocytosis is a major unappreciated driver of lesion

173 e of apoptotic cells by wound macrophages or efferocytosis is a prerequisite for the timely resolutio

174 Impaired efferocytosis is associated with an unfavorable outcome

175 ed that apoptotic cell clearance activity or efferocytosis is compromised in diabetic wound macrophag

176 Because efferocytosis is critical for the resolution of inflamma

177 Because efferocytosis is defective in many of the same illnesses

178 rther show that the specific role of PALL in efferocytosis is driven by its apoptotic cell-induced nu

179 important therapeutic role in diseases where efferocytosis is impaired and inflammation is dysregulat

180 Genetic and experimental data suggest that efferocytosis is impaired during atherogenesis caused by

181 Macrophage efferocytosis is known to trigger the release of anti-in

182 Efferocytosis is mediated, in part, by receptors that bi

183 While efferocytosis is recognized as a constitutive housekeepi

184 We suggest that efferocytosis is regulated in an autocrine manner by pro

185 The clearance of apoptotic cells (i.e. efferocytosis) is a key modulator of the immune response

186 Because phagocytosis of apoptotic cells (efferocytosis) is a pivotal regulator of inflammation, w

187 Efficient clearance of apoptotic cells (efferocytosis) is a prerequisite for inflammation resolu

188 Clearance of apoptotic cells (efferocytosis) is achieved through phagocytosis by profe

189 Apoptotic cell (AC) clearance (efferocytosis) is an evolutionarily conserved process es

190 s that efficient removal of apoptotic cells (efferocytosis) is bolstered in the presence of wild-type

191 clearance of apoptotic cells by phagocytes (efferocytosis) is critical for normal tissue homeostasis

192 Clearance of apoptotic cells (efferocytosis) is critical to the homeostasis of the imm

193 rticular, the clearance of apoptotic bodies (efferocytosis) is enabled by externalization on the cell

194 Apoptotic cell phagocytosis (efferocytosis) is mediated by specific receptors and is

195 clearance of apoptotic cells by macrophages (efferocytosis) is thought to lead to increased necrotic

196 Phagocytosis of apoptotic cells, also called efferocytosis, is an essential feature of immune respons

197 Phagocytosis of apoptotic cells, also called efferocytosis, is an essential feature of immune respons

198 tic M. tuberculosis (Mtb)-infected cells, or efferocytosis, is considered beneficial for host defense

199 imely clearance by macrophage engulfment, or efferocytosis, is critical for efficient tissue repair.

200 ells by phagocytes, a process referred to as efferocytosis, is essential for maintenance of normal ti

201 The elimination of apoptotic cells, called efferocytosis, is fundamentally important for tissue hom

202 rs and intracellular signaling components of efferocytosis, its negative regulation remains incomplet

203 , suggesting that therapeutically augmenting efferocytosis may improve functional outcomes by both re

204 significance of miR-21 in the regulation of efferocytosis-mediated suppression of innate immune resp

205 ytosis of ACM and that strategies to enhance efferocytosis might attenuate diabetes-induced impairmen

206 his process, termed glucocorticoid-augmented efferocytosis, might explain the association of CAP with

207 study demonstrates that following successful efferocytosis, miR-21 induction in macrophages silences

208 Namely, TAM-mediated efferocytosis, negative regulation of dendritic cell act

209 These data suggests that diabetes impairs efferocytosis of ACM and that strategies to enhance effe

210 In the present study we found that invitro efferocytosis of ACM was impaired in macrophages from db

211 he effect of diabetes on macrophage-mediated efferocytosis of apoptotic cardiomyocytes (ACM) and the

212 Successful efferocytosis of apoptotic cells by monocyte-derived mac

213 ort that macrophage- and neutrophil-mediated efferocytosis of apoptotic cells containing mycobacteria

214 cantly increased murine and human macrophage efferocytosis of apoptotic cells, independent of macroph

215 terial phagocytosis and clearance as well as efferocytosis of apoptotic cells.

216 BCCs), there was a robust enhancement in the efferocytosis of apoptotic cells.

217 Efferocytosis of apoptotic neutrophils by macrophages fo

218 The efferocytosis of apoptotic neutrophils by macrophages pr

219 Phagocytosis of B. burgdorferi and efferocytosis of apoptotic neutrophils was defective in

220 ges toward resolving phenotypes and enhanced efferocytosis of apoptotic neutrophils.

221 easing proinflammatory mediators, increasing efferocytosis of apoptotic PMNs, and stimulating local e

222 MEKi-treated mice had increased efferocytosis of apoptotic polymorphonuclear leukocytes

223 greatly impaired phagocytosis of zymosan and efferocytosis of apoptotic thymocytes following epoxI tr

224 The molecular mechanisms of efferocytosis of cardiomyocytes and in the myocardium ar

225 sine kinase was necessary and sufficient for efferocytosis of cardiomyocytes ex vivo.

226 eptor tyrosine kinases AXL and MERTK reduced efferocytosis of eryptotic erythrocytes and hematoma cle

227 Thus, our results identify the efferocytosis of eryptotic erythrocytes through AXL/MERT

228 Efferocytosis of M. tuberculosis sequestered within an a

229 ated that LPS and TNF-alpha potently inhibit efferocytosis of neutrophils by monocyte-derived Mphis.

230 ined whether uPAR plays a role in modulating efferocytosis of neutrophils.

231 is study, we observed that macrophage-driven efferocytosis of prostate cancer cells in vitro induced

232 The impaired recognition and removal (efferocytosis) of apoptotic neutrophils by CGD macrophag

233 tosis and defective phagocytic clearance, or efferocytosis, of the apoptotic macrophages.

234 hat the phagocytic clearance of dying cells (efferocytosis), particularly by macrophages and other im

235 For efficient efferocytosis, phagocytes must be able to internalize mu

236 g mediators of inflammation drive macrophage efferocytosis (phagocytosis of apoptotic cells) and reso

237 ular mechanism that contributes to defective efferocytosis, plaque necrosis, and impaired resolution

238 e data suggest that PTEN exerts control over efferocytosis potentially by regulating PtdIns(3,4,5)P(3

239 Importantly, suppressed efferocytosis preceded increases in myocardial infarct s

240 ance of apoptotic cells (ACs) by phagocytes (efferocytosis) prevents post-apoptotic necrosis and damp

241 stigated the hypothesis that MFG-E8-mediated efferocytosis promotes M2 polarization.

242 terial phagocytes to uptake apoptotic cells (efferocytosis) promotes lesion growth and establishment

243 We further demonstrate that the efferocytosis-promoting activity essentially required th

244 role for RpS6 in the negative regulation of efferocytosis provides the opportunity to develop new st

245 that proteolytic cleavage of the macrophage efferocytosis receptor c-Mer tyrosine kinase (MerTK) red

246 with increased expression of the macrophage efferocytosis receptor MerTK.

247 acrophage PPARgamma-mediated programming and efferocytosis, reduced accumulation of apoptotic neutrop

248 /ob and ob/ob;Ldlr(-/-) mice showed impaired efferocytosis, reflecting defective phosphatidylinositol

249 a significant increase in expression of the efferocytosis-regulating integrin-beta3 and its ligand m

250 e of ADAM17-mediated proteolysis for in vivo efferocytosis regulation and suggest a possible mechanis

251 We review specific types of efferocytosis-related signals that can impact macrophage

252 h Ccn1 knockdown are defective in neutrophil efferocytosis, resulting in exuberant neutrophil accumul

253 effect of Scnn(+) bronchoalveolar lavage on efferocytosis, showing that this effect is due to HMGB1.

254 ogeneity of phagocyte populations influences efferocytosis signaling, and downstream consequences of

255 f the cleavage product soluble Mer, improved efferocytosis, smaller necrotic cores, thicker fibrous c

256 6 axis is a positive regulator of macrophage efferocytosis, survival, and phenotypic conversion, dire

257 Kumar and Birge introduce efferocytosis - the process by which dead or dying cells

258 s of alternatively activated macrophages and efferocytosis, the extra-mesenchymal origin of fibroblas

259 the coordinated role of 2 major mediators of efferocytosis, the myeloid-epithelial-reproductive prote

260 hat this phenomenon is caused by a defect in efferocytosis, the process by which apoptotic tissue is

261 Efferocytosis, the process by which dying or dead cells

262 ion-induced membrane damage as a trigger for efferocytosis, the recognition and uptake of dead cells,

263 Given the ability of efferocytosis to polarize ingesting Mo uniquely and to r

264 athogen, Listeria monocytogenes, can exploit efferocytosis to promote cell-to-cell spread during infe

265 These data collectively and directly link efferocytosis to wound healing in the heart and identify

266 Given the immunomodulatory properties of efferocytosis, understanding pathways that regulate and

267 IL-4-dependent macrophage reprogramming and efferocytosis via a similar mechanism.

268 is, we hypothesized that 5-HT would suppress efferocytosis via activation of RhoA/ROCK.

269 Importantly, CS profoundly inhibited AM efferocytosis via ceramide-dependent sphingosine product

270 These results uncover a unique role of efferocytosis via MFG-E8 as a mechanism for macrophage p

271 icoids reversed inhibitory effects of LPS on efferocytosis via suppression of TNF-alpha production.

272 The effect of ceramide on efferocytosis was associated with decreased membrane ruf

273 The effect of 5-HT on efferocytosis was examined in murine peritoneal and huma

274 A similar defect in efferocytosis was induced by treating control macrophage

275 The effect of lovastatin on efferocytosis was investigated in primary human macropha

276 ffect of endogenous or exogenous oxidants on efferocytosis was mediated through activation of the GTP

277 tory macrophages and their activities (e.g., efferocytosis) was also implicated in exacerbated inflam

278 way, either the enhancement or inhibition of efferocytosis, was exquisitely sensitive to concentratio

279 ng shown that ICS significantly increase AMo efferocytosis, we hypothesized that this process, termed

280 tosis of Escherichia coli and apoptotic PMN (efferocytosis) were enhanced with GPR18 overexpression a

281 terleukin 4 (IL-4) normalized CGD macrophage efferocytosis, whereas classical activation by lipopolys

282 nt or genetic knockdown of miR-34a increased efferocytosis, whereas miR-34a overexpression decreased

283 hil apoptosis, macrophage reprogramming, and efferocytosis, which have a major impact on the establis

284 ugh receptor tyrosine kinase MerTK-dependent efferocytosis, which robustly induced the transcription

285 se lesions demonstrated evidence of enhanced efferocytosis, which was associated with increased expre

286 is, whereas miR-34a overexpression decreased efferocytosis, without altering recognition of live, nec