ライフサイエンスコーパス: efferocytosis

1 through a specialized form of phagocytosis (efferocytosis).

2 to effective apoptotic neutrophil clearance (efferocytosis).

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

4 ocytes (PMNs), followed by PMN apoptosis and efferocytosis.

5 apoptotic cancer cells in a process known as efferocytosis.

6 bca1, three proteins that promote macrophage efferocytosis.

7 nsibility of macrophages in a process called efferocytosis.

8 gnaling within macrophages to prime them for efferocytosis.

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

10 h specifically regulates and is regulated by efferocytosis.

11 phage cholesterol homeostasis with defective efferocytosis.

12 ented CM-induced MerTK cleavage and promoted efferocytosis.

13 of DD1alpha, two proteins known to influence efferocytosis.

14 d we found no evidence of defective lesional efferocytosis.

15 as associated with significant inhibition of efferocytosis.

16 is signaling, and downstream consequences of efferocytosis.

17 d leads to macrophage death and insufficient efferocytosis.

18 gocytosis, phagolysosomal acidification, and efferocytosis.

19 he engulfment of apoptotic bodies, so-called efferocytosis.

20 vbeta3/alphavbeta5 in macrophages to trigger efferocytosis.

21 ivation and F-actin remodeling that promotes efferocytosis.

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

23 D1 and D3 reduced inflammation by promoting efferocytosis.

24 es its dissemination in a host by exploiting efferocytosis.

25 are required at least for the initiation of efferocytosis.

26 ant but lesser roles in antigen sampling and efferocytosis.

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

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

29 e lipid-laden necrotic core through impaired efferocytosis.

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

31 ignaling required for membrane expansion and efferocytosis.

32 mulated each other's expression and enhanced efferocytosis.

33 had equally important inhibitory effects on efferocytosis.

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

35 of dead and dying cells, a process known as efferocytosis.

36 k between chronic inflammation and defective efferocytosis.

37 ly activated (M2) macrophages and neutrophil efferocytosis.

38 associated with impaired macrophage/monocyte efferocytosis.

39 uPAR or Abs to uPAR significantly diminished efferocytosis.

40 apoptotic cells by phagocytes is defined as efferocytosis.

41 icles contributed to SPM biosynthesis during efferocytosis.

42 nd the immunological consequences of in situ efferocytosis.

43 idylinositol 3-phosphatase, is elevated upon efferocytosis.

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

45 ease activity and NET formation and modifies efferocytosis.

46 rs and phagocytosed through a process termed efferocytosis.

47 monophosphate, phagocytosis of bacteria, and efferocytosis.

48 llular process of inflammation-resolution is efferocytosis.

49 upstream of SLC12A2-had a similar effect on efferocytosis.

50 capacity to phagocyte-damaged neutrophils by efferocytosis.

51 expansion of the necrotic core by impairing efferocytosis.

52 erythrocytes and polymorphonuclear leukocyte efferocytosis, (2) blunting of NF-kappaB activation, and

53 new role for ICAM-1 in promoting macrophage efferocytosis, a critical process in the resolution of i

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

55 Efferocytosis, a process of clearance of apoptotic cells

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

57 es was also impaired, leading to inefficient efferocytosis, accumulation of apoptotic cardiomyocytes,

58 t cancer that necrosis secondary to impaired efferocytosis activates IDO1 to drive immunosuppression

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

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

61 ocytosis, and responses of phagocytes during efferocytosis, all of which can alter the homeostatic ti

62 aired clearance of neutrophils by monocytes (efferocytosis) allowing prolonged neutrophil persistence

63 Efferocytosis also limits tissue damage by increasing im

64 e of Mertk function on macrophages decreased efferocytosis, altered the cytokine milieu, and resulted

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

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

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

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

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

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

71 The defect in efferocytosis and elevated apoptosis sensitivity of APOE

72 tion and plaque apoptotic cells and promotes efferocytosis and features of stable plaques.

73 Combined inhibition of efferocytosis and IDO1 in tumor residual disease decreas

74 that apoptotic and necrotic tumor cells, via efferocytosis and IDO1, respectively, promote tumor 'hom

75 strategies for diseases driven by defective efferocytosis and impaired inflammation resolution.

76 s better understand the relationship between efferocytosis and inflammation.

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

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

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

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

81 biological functions including regulation of efferocytosis and leukocyte trafficking.

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

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

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

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

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

87 m myelopoiesis over leukocyte recruitment to efferocytosis and resolution of inflammation).

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

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

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

91 ing apoptotic cell uptake; the links between efferocytosis and the resolution of inflammation in heal

92 ximizes PS receptor-mediated virus entry and efferocytosis and underscore the important contribution

93 izes with PS to enhance PS receptor-mediated efferocytosis and virus entry.

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

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

96 flammation, impaired SPM:LT ratio, defective efferocytosis, and a decrease in MerTK levels in injured

97 cells had increased MerTK cleavage, impaired efferocytosis, and a defective RvD1:LTB(4) ratio.

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

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

100 1, reversed the inhibitory effect of 5-HT on efferocytosis, and decreased cellular peritoneal inflamm

101 a coli in mice and suppresses PMN apoptosis, efferocytosis, and generation of proresolving lipid medi

102 es, MaR1 (0.01-10 nM) enhanced phagocytosis, efferocytosis, and phosphorylation of a panel of protein

103 mitigated I/R lung injury in aging, promoted efferocytosis, and prevented the decrease of MerTK in in

104 to the clearance of neutrophils, stimulating efferocytosis, and promoting epithelial repair.

105 achinery, disruptions at different stages of efferocytosis, and responses of phagocytes during effero

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

107 'eat' apoptotic leukocytes, a process called efferocytosis, and thereby promote an anti-inflammatory

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

109 onse, alternative activation of macrophages, efferocytosis, and upregulation of specialized proresolv

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

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

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

113 ession in TME via upregulation of GM-CSF and efferocytosis as well as deregulation of lipid metabolis

114 Defective efferocytosis, as a sign of inadequate inflammation reso

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

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

117 Although many efferocytosis-associated receptors have been described i

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

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

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

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

122 Efferocytosis by airway macrophages was assessed in obes

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

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

125 rgo of dead and dying cells ingested through efferocytosis by macrophages can alter metabolic pathway

126 Efferocytosis by macrophages was 40% lower in obese than

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

128 5-HT impaired efferocytosis by murine peritoneal macrophages and human

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

130 rated an antibody that selectively inhibited efferocytosis by phagocytic receptor MerTK.

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

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

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

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

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

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

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

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

139 ceptors mediate clearance of apoptotic cells-efferocytosis-by recognizing the PS exposed on those cel

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

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

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

143 We report here that efferocytosis cleared apoptotic tumor cells in residual

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

145 nuclear cells infiltration and had improved efferocytosis compared with old WT controls.

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

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

148 MerTK(CR) mice were resistant to CM-induced efferocytosis defects and had an improved RvD1:LTB(4) ra

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

150 Defective efferocytosis drives important diseases, including ather

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

152 mice reduced macrophage CD206 expression and efferocytosis during peritonitis.

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

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

155 Apoptotic cell clearance (efferocytosis) elicits an anti-inflammatory response by

156 agocytic clearance of apoptotic tumor cells (efferocytosis) enhances the immunosuppressive function o

157 Thus, tumor cell efferocytosis following cytotoxic cancer treatment could

158 Here, we outline the mechanisms of efferocytosis, from the recognition of dying cells throu

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

160 sed lung neutrophil apoptosis and macrophage efferocytosis in a murine acute lung injury model.

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

162 erapy to promote inflammation-resolution and efferocytosis in aging.

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

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

165 tion in health and disease; and the roles of efferocytosis in host defence.

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

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

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

169 creasing macrophage apoptosis and increasing efferocytosis in the vessel wall.

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

171 itical regulator of macrophage apoptosis and efferocytosis in vitro, in an HuR-dependent manner.

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

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

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

175 oid the pathologic consequences of defective efferocytosis in vivo.

176 before intratracheal instillation decreased efferocytosis in vivo.

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

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

179 Efferocytosis increased specialized pro-resolving mediat

180 rophages exhibited a significantly bolstered efferocytosis index.

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

182 DEL-1-mediated efferocytosis induced liver X receptor-dependent macroph

183 Blockade of efferocytosis induced secondary necrosis of apoptotic ce

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

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

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

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

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

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

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

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

192 Because efferocytosis is defective in many of the same illnesses

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

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

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

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

197 Efferocytosis is performed by macrophages and to a lesse

198 While efferocytosis is recognized as a constitutive housekeepi

199 Efferocytosis is the process by which apoptotic cells ar

200 -professional phagocytes - a process termed 'efferocytosis' - is essential for the maintenance of tis

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

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

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

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

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

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

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

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

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

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

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

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

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

214 in inflammation and injury, a process termed efferocytosis, it was examined whether ICAM-1 contribute

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

216 hog; how clearance of dead cells in NASH via efferocytosis may affect inflammation and fibrogenesis;

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

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

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

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

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

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

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

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

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

226 Successful efferocytosis of apoptotic cells by monocyte-derived mac

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

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

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

230 human monocyte-derived macrophages enhanced efferocytosis of apoptotic human neutrophils.

231 Efferocytosis of apoptotic neutrophils (PMNs) by alveola

232 Efferocytosis of apoptotic neutrophils by macrophages fo

233 The efferocytosis of apoptotic neutrophils by macrophages pr

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

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

236 TSG6- or IL-4-primed BMM s induced efferocytosis of apoptotic PMNs compared with control BM

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

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

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

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

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

242 The release of mito-DAMPs is controlled by efferocytosis of dying hepatocytes by phagocytic residen

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

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

245 Efferocytosis of M. tuberculosis sequestered within an a

246 macrophage phenotype transition resulting in efferocytosis of PMNs plays a crucial role in the resolu

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

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

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

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

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

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

253 Importantly, suppressed efferocytosis preceded increases in myocardial infarct s

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

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

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

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

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

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

260 with increased expression of the macrophage efferocytosis receptor MerTK.

261 Ablation of a canonical efferocytosis receptor, MerTK, blunted efferocytic signa

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

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

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

265 ngulfment of apoptotic cells by macrophages (efferocytosis) resolves inflammation via a miR-21-PDCD4-

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

267 Understanding these aspects of efferocytosis sheds light on key physiological and patho

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

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

270 We found that efferocytosis stimulated expression of IFN-gamma, which

271 6 axis is a positive regulator of macrophage efferocytosis, survival, and phenotypic conversion, dire

272 idly removed by phagocytes by the process of efferocytosis that is anti-inflammatory.

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

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

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

276 Efferocytosis, the process by which dying or dead cells

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

278 accumulation, and promotes PMN apoptosis and efferocytosis, thereby facilitating resolution of E. col

279 olecules involved in the different phases of efferocytosis to disease pathologies that can arise due

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

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

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

283 Efferocytosis transcriptionally altered the genes that e

284 Efferocytosis triggers cellular reprogramming, including

285 Accordingly, defective efferocytosis underlies a growing list of chronic inflam

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

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

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

289 Decreased efferocytosis was also seen in vitro and in vivo with in

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

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

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

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

294 define the transcriptional diversity during efferocytosis, we utilized single-cell mRNA sequencing a

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

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

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

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

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

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