ライフサイエンスコーパス: macrophage

1 ines an adaptive homeostasis in the infected macrophage.

2 n of innate memory in activated NK cells and macrophages.

3 leading to restriction of HIV replication in macrophages.

4 ist in tissues within granulomas composed of macrophages.

5 in the main population of resident vascular macrophages.

6 sis, and the infiltration of pro-tumorigenic macrophages.

7 ng to aerobic glycolysis and polarization of macrophages.

8 elevated pro-inflammatory gene expression in macrophages.

9 maintenance factor expression in bone marrow macrophages.

10 erpart of these cells to be monocyte-derived macrophages.

11 1) as one of the top genes induced by PM in macrophages.

12 s IL-10 production by human monocyte-derived macrophages.

13 rancisella tularensis, that infects alveolar macrophages.

14 infectious amastigote forms inside mammalian macrophages.

15 s sufficient for REAF degradation in primary macrophages.

16 ain induced less IL-10, but higher IL-12, in macrophages.

17 between a microglia cluster and infiltrating macrophages.

18 expression of arginase-1 and YM1 in primary macrophages.

19 lammation from galactosylceramide storage in macrophages.

20 involving activation of the inflammasome in macrophages.

21 important for efficient infection of primary macrophages.

22 a subset of tumor-infiltrating M2-polarized macrophages.

23 mulates an increase in O-GlcNAc signaling in macrophages.

24 ing to an accumulation of significantly more macrophages.

25 ominantly infect respiratory epithelium, not macrophages.

26 er, the cells do not transdifferentiate into macrophages.

27 in Mycobacterium tuberculosis (Mtb)-infected macrophages.

28 P-1 cells and primary human monocyte-derived macrophages.

29 ce of fluid and cells, including profibrotic macrophages.

30 sponse genes including BiP, CHOP, and PDI in macrophages.

31 e response and increasing tumor infiltrating macrophages.

32 ally, Smyd2 was induced by c-Myc in infected macrophages.

33 LR ligand binding than their closely related macrophages.

34 CCR5) in T cells and CD4 in both T cells and macrophages.

35 effector molecule regulating Mtb survival in macrophages.

36 attenuates pro-inflammatory gene programs in macrophages.

37 llular phenotype of injected tissue-resident macrophages.

38 those of wild-type bacteria in the infected macrophages.

39 ) infection induce GBP2 expression in murine macrophages.

40 1/2 and ERK-1/2 in BALB/c-derived peritoneal macrophages.

41 tsia australis activates ASC inflammasome in macrophages.

42 L receptor increased the DR cell population, macrophage accumulation, and hepatic fibrosis in the Mdr

43 e show that D-mannose suppresses LPS-induced macrophage activation by impairing IL-1beta production.

44 to maintain the negative feedback control of macrophage activation in response to bacterial infection

45 in response to Ifn-gamma during CpG-induced macrophage activation syndrome and is present at high le

46 ammatory disorders and is usually designated macrophage activation syndrome in those settings.

47 n be damaging to the host, as is seen in the macrophage activation syndrome induced by severe infecti

48 with a cytokine signature similar to that of macrophage activation syndrome/hemophagocytic lymphohist

49 ated lesions with axonal loss and microglial/macrophage activation were also observed.

50 The ontogeny of airway macrophages (AMs) in human lung and their contribution t

51 Interestingly, alveoli outnumber alveolar macrophages (AMs), which favors alveoli devoid of AMs.

52 In the current study, we defined "M1" macrophage and "M1"/"M2" ratio by transcriptomic signatu

53 In cerebrospinal fluid (CSF), we measured 3 macrophage and microglia-related proteins, chitotriosida

54 li LPS may increase liver damage by inducing macrophage and platelet activation through the TLR4 path

55 cts of cottonseed extracts in mouse RAW264.7 macrophages and 3T3-L1 adipocytes.

56 as important for parasite infection of host macrophages and a potential therapeutic target.

57 d amastigote multiplication in infected J774 macrophages and BALB/c mice, respectively.

58 alose decreased viral entry in human primary macrophages and CD4(+) T cells through the downregulatio

59 is essential for reprogramming interstitial macrophages and dampening inflammatory injury.

60 and unique features between neural resident macrophages and emphasize the role of nerve environment

61 associated with inflammatory polarization of macrophages and fibroblasts.

62 Furthermore, macrophages and fibulin-2 levels were reduced in stroma

63 pts the proliferation of bone marrow-derived macrophages and granulocytes.

64 lyase (Acly) to be activated in inflammatory macrophages and human atherosclerotic plaques.

65 of the DUB mutant virus (DUBmut) in cultured macrophages and in mice.

66 model conditions such as growth in vitro, in macrophages and in the mouse.

67 ated with increased numbers of CD68 and F480 macrophages and increased clearance of damaged hepatocyt

68 a functional 5-HT/5-HT(2B)/AhR axis in human macrophages and indicate that 5-HT potentiates the activ

69 lia only in patients with COPD and monocytes/macrophages and lymphocytes in both patients with COPD a

70 tory (GM-CSF-treated) human monocyte-derived macrophages and microglia using RNA sequencing.

71 t Mtb growth more efficiently than all other macrophages and monocytes despite equivalent infections

72 glucan treatment reduced c-MAF expression in macrophages and monocytes from patients with non-small c

73 sed severe inflammation with infiltration of macrophages and neutrophils and upregulation of pro-infl

74 ngs reveal that the combined infiltration of macrophages and neutrophils is required for autoreactive

75 ls convey resistance to CDC-induced pores on macrophages and neutrophils.

76 he canonical DZ that contained tingible body macrophages and were sites of ongoing cell division.

77 els of calreticulin (the "eat me" signal for macrophages) and high levels of CD47 (the "do not eat me

78 vels of CD47 (the "do not eat me" signal for macrophages) and PD-L1 (a T-cell inactivator) on their s

79 mmation, notably via granulocytes, monocytes/macrophages, and CD1a(int)-expressing cell recruitment.

80 circulating blood monocytes, resident tissue macrophages, and dendritic cells (DCs) present in every

81 trate that lytic MHV68 infection of B cells, macrophages, and fibroblasts leads to robust activation

82 flammatory cell infiltration (CD3 + T cells, macrophages, and neutrophils), elastic fiber disruption,

83 the efflux of radiolabeled UC from cultured macrophages, and, in the simultaneous presence of HDL, a

84 These findings implicate the involvement of macrophage AQP3 in liver injury, and provide evidence fo

85 Lung macrophages are important in mounting an inflammatory re

86 Endothelial cells and macrophages are likely targets as these cell types highl

87 K) cells, NKT cells, gammadelta T cells, and macrophages, are promising alternatives to alphabeta CAR

88 If AMs, like most tissue macrophages, are sessile, then this numerical advantage

89 identify a macrophage-specific lncRNA MAARS (Macrophage-Associated Atherosclerosis lncRNA Sequence).

90 expression of Mrc1 and Chil1, markers of M2 macrophages at the MI zone.

91 hages, collectively termed border-associated macrophages (BAMs).

92 ate the pathogenesis of UC and summarize the macrophage-based nanotherapeutic strategies in UC.

93 ith exciting opportunities for the future of macrophage-based therapies in oncology are included.

94 tool may be of great value for the study of macrophage biology in different organs and various model

95 Bone marrow-derived macrophages (BMDMs) are recruited to the injured myocard

96 nhibited the spread of LVS infection between macrophages, but bacteria did not return to vacuoles suc

97 LRP3-dependent caspase-1 activation of human macrophages, but not for TLR2 signaling.

98 masome activation and IL-1beta production in macrophages by detoxifying excessive ROS levels.

99 hage phagocytosis allowing repression of rat macrophages by human CD47-positive cells.

100 ses long-term changes in bone marrow-derived macrophages by suppressing interleukin 1beta, CD68, and

101 Proinflammatory M1 macrophages can phagocytose tumor cells, while anti-infl

102 Aberrant NLRC5 signaling in macrophages can promote B-cell lymphomagenesis during ch

103 CAR macrophages (CAR-Ms) demonstrated antigen-specific phago

104 The activated macrophages caused stellate cell activation, leading to

105 in glaucomatous eyes also indicate that ILM macrophage cells appear to play an early and regionally

106 re we examine key characteristics of retinal macrophage cells in live human eyes, both healthy and di

107 ellular phospho-STAT3 levels in J774.2 mouse macrophage cells.

108 ndependent of protein expression within live macrophage cells.

109 in vitro BBB model and suppress the HIV-1 in macrophage cells.

110 ocytes and inflammatory cells, like monocyte/macrophages, cellular settings where these epigenetic re

111 evealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with

112 ges, known as microglia, and non-parenchymal macrophages, collectively termed border-associated macro

113 Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a multi

114 Granulocyte-macrophage colony-stimulating factor (GM-CSF) signalling

115 Granulocyte-macrophage colony-stimulating factor (GM-CSF), a myelopo

116 by reducing the expression and secretion of macrophage colony-stimulating factor CSF1 by tumor cells

117 ting factor receptor family (CSF3R/CSF3) and macrophage colony-stimulating factor receptor family (CS

118 tumor burden and infiltration of MDSC and M2 macrophages compared with LNs at other sites.

119 red the phenotypes of colonic lamina propria macrophages, compared with wild-type mice.

120 Macrophages comprise a majority of the resident immune c

121 type characterized by an increased lipid and macrophage content, plaque size, and pro-inflammatory cy

122 urthermore, it promoted the precursors of M2 macrophages, DCs and regulatory T cells.

123 of immune pressure, eventually resulting in macrophage death.

124 Macrophages demonstrate remarkable plasticity that is es

125 3-mediated H(2)O(2) transport as therapy for macrophage-dependent liver injury.

126 e csf1r-deficient zebrafish exhibit systemic macrophage depletion.

127 ervation in both sexes, specifically whether macrophage-derived vascular endothelial growth factor-A

128 ulomas surrounded by proinflammatory M1-like macrophages developed late in this process of chronic UA

129 oles such as lysosomes or autophagosomes and macrophages did not die.

130 In fact, pro- and anti-inflammatory macrophages differ in the expression of serotonin recept

131 ct effect of IL-33-ST2 signaling on monocyte/macrophage differentiation, self-renewal and repairing a

132 regeneration, which fully restored original macrophage distributions and morphologies.

133 helper 1 response, alternative activation of macrophages, efferocytosis, and upregulation of speciali

134 data were particularly enriched in lesional macrophages, endothelial, and smooth muscle cells.

135 fic uptake in inflamed myocardium containing macrophages expressing FR-beta, which were also present

136 acity when cultured with FFA, whereas female macrophages failed to migrate.

137 confirmed that SIRPalpha not only restrains macrophages from acquiring a hemophagocytic phenotype bu

138 tants MIP-2alpha and CXCL5 in AAA lesions or macrophages from Apoe(-/-) Ige(-/-) mice, along with red

139 ne storm syndrome pathogenesis by preventing macrophages from becoming both hemophagocytic and hypera

140 pendent rescue of HIV-1 replication in human macrophages from inhibition by cGAMP, the product of act

141 Macrophages from male mice maintained migratory capacity

142 his response was lost in bone marrow-derived macrophages from mice deficient in AMPK (Prkab1(-/)(-))

143 the relative composition of CD14(+)CD11c(+) macrophages from mucus in two phyla (Proteobacteria [p =

144 protein, however, has a role in normal human macrophage function has not been determined.

145 y inflammatory response to LPS by regulating macrophage function, suggesting an essential role of thi

146 uncated O-linked glycans and their receptor, macrophage galactose-type lectin (MGL), on CD163(+) TAMs

147 e growth factor-1), and the splenic red pulp macrophage gene Spic.

148 oreover, cadmium exposure promoted increased macrophage glycolytic function with enhanced extracellul

149 Macrophages have been linked to ductal development in th

150 Furthermore, macrophages have low/no basal expression of ST2.

151 In mouse bone marrow-derived macrophages, heme induced HO-1, lipid regulatory genes i

152 cytokine, plays a critical role in alveolar macrophage homeostasis, lung inflammation and immunologi

153 RNA sequencing of morphologically distinct macrophages identified LXR/RXR as the most enriched path

154 he role of nerve environment for shaping PNS macrophage identity.

155 gA2 acts pro-inflammatory on neutrophils and macrophages, IgA1 does not have pronounced effects.

156 the increasing understanding of the roles of macrophage immunometabolism in atherosclerosis, new exci

157 tence of intact N4BP1 in caspase-8-deficient macrophages impairs their ability to mount robust cytoki

158 factor, REAF, that impedes HIV infection in macrophages.IMPORTANCE For at least 30 years, it has bee

159 leading to restriction of HIV replication in macrophages.IMPORTANCE HIV continues to be a major publi

160 feration of T. cruzi amastigotes in infected macrophages in a concentration-dependent manner and demo

161 of these anti-inflammatory, growth-promoting macrophages in a human infectious disease, biopsies from

162 nscriptional and epigenetic heterogeneity of macrophages in atherosclerotic plaques.

163 in the microglia but not bone marrow-derived macrophages in both in vitro and in vivo GBM mouse model

164 fect the immune microenvironment, especially macrophages in clearing dying hepatocytes.

165 porting adhesion of cultured human and mouse macrophages in experiments using recombinant TSP4 varian

166 nchymal microglia and extraparenchymal brain macrophages in homeostasis and during disease.

167 iac sarcoidosis showed many FR-beta-positive macrophages in inflammatory lesions.

168 ry metabolic and epigenetic reprogramming of macrophages in N-ERD.

169 crophages predominant in lean AT and M1-like macrophages in obese AT.

170 Unexpectedly, depletion of macrophages in obese mice enhanced mammary epithelial ce

171 modulated to facilitate protein secretion in macrophages in response to LPS.

172 cted mice with persistent CD11b(+) microglia/macrophages in the inflamed regions on day 30 p.i.

173 quiline (BDQ) is localised not only in foamy macrophages in the lungs during infection but also accum

174 PnV increased the number of macrophages in the tumor, while did not increase in the

175 Human monocytes and mouse macrophages in tumor cocultures exhibited significantly

176 is directly involved in the polarization of macrophages in vitro and in vivo, including the up-regul

177 M-induced inflammation or NRF2 activation in macrophages in vitro or in vivo.

178 r understand the latter, we stimulated human macrophages in vitro with TLR ligands in the presence of

179 The effect of venom was also evaluated on macrophages in vitro.

180 Finally, the developing field of engineered macrophages, including genetic engineering and integrati

181 t were adjacent to [(13)C]cholesterol-loaded macrophages-including in cytosolic lipid droplets of SMC

182 Nevertheless, Legionella-infected macrophages induce an interleukin-1 (IL-1)-dependent inf

183 tly upregulated C-type lectin receptor (CLR) macrophage-inducible Ca2+-dependent lectin receptor (Min

184 PD-L1; (3) PD-L1(+) T cells engaged PD-1(+) macrophages, inducing an alternative M2-like program, wh

185 genes regulated by SpxA1 in broth and during macrophage infection.

186 pendent DNA sensor pathway, which results in macrophage infiltration and activation during Kras-drive

187 MI, lack of Gal-3 markedly attenuated F4/80+ macrophage infiltration and significantly increased the

188 gesting an essential role of this pathway in macrophage inflammatory response.

189 Furthermore, blockage of nSMase in monocytes/macrophages inhibited the secretion of inflammatory medi

190 cancer, malignant cells recruit and educate macrophages into a M2 tumor-promoting phenotype that sup

191 ity of iron at the phagosomal surface inside macrophage is crucial for survival and virulence of M. t

192 The central nervous system hosts parenchymal macrophages, known as microglia, and non-parenchymal mac

193 Sema3E high-affinity receptor, plexinD1, on macrophages led to the improvement in clinical disease f

194 mor-infiltrating slan(+) -cells, including a macrophage-like state.

195 nscriptomes of monocyte-like THP-1 cells and macrophage-like THP-1 cells (THP1-MPhi) have largely con

196 infected cell types included CD68(+) type A (macrophage-like) synoviocytes and CD44(+) type B (fibrob

197 Cells of the monocyte/macrophage lineage play a key role in providing chemokin

198 restricted to M-CSF-primed monocyte-derived macrophages (M-MO).

199 eeks) had reductions in MDC (mainly CD11c(+) macrophage) M1-like polarization and interferon-gamma-ex

200 ion (classically and alternatively activated macrophages: M1 and M2, respectively) were studied using

201 Loss of ATP sensing in macrophages may reduce their secretory capacity.

202 in macrophage-mediated immune modulation and macrophage-mediated drug delivery, which will further en

203 is still significant room for development in macrophage-mediated immune modulation and macrophage-med

204 SARS-CoV-2 may modulate macrophage-mediated inflammation events by altering the

205 and hypertension may synergistically induce macrophage metabolic dysfunction, particularly during ca

206 rent status of potential therapies to target macrophage metabolism during heart failure, including an

207 However, relative to macrophages/microglia, comparatively less is known about

208 d the pivotal role of the versatile cytokine macrophage migration inhibitory factor (MIF) in regulati

209 The alternative endogenous ligand macrophage migration inhibitory factor behaves opposite

210 ly, DPP4 mediated the glucocorticoid-induced macrophage migration, and siRNA-mediated knockdowns of G

211 Of note, glucocorticoids highly stimulated macrophage mobility; unexpectedly, DPP4 mediated the glu

212 inflammatory cytokine production, and making macrophages more susceptible to receiving suppressive si

213 ed in P2-deficient mouse bone marrow-derived macrophages, mouse embryonic fibroblasts (MEFs), and hum

214 Beyond macrophages, neutrophils also accumulate in adipose and

215 Here, we show that macrophages not only fail to efficiently kill phagocytos

216 Both macrophage number and Vegf-A expression increased in end

217 Macrophage numbers were significantly decreased in sever

218 the population of resident and interstitial macrophages of peritoneum, lung, and liver but not splee

219 exciting findings on microglia, the resident macrophages of the central nervous system (CNS).

220 Microglia are parenchymal macrophages of the CNS; as professional phagocytes they

221 , but less is known regarding the effects of macrophages on the adipose stroma.

222 ures (modules) for differentially stimulated macrophages, one to assess lung tissue-resident cells (T

223 0126 or genetically with bone marrow-derived macrophages or DCs from Tpl2(-/-) mice.

224 dies, suggesting that M-tropic viruses had a macrophage origin.

225 hich cells were rested and differentiated to macrophages over 5 days.

226 ning regulatory T cells, dendritic cells, or macrophages; patient selection and immunosuppression mir

227 mulating factor 1 receptor (CSF1R), but some macrophages persist in the absence of CSF1R.

228 atory protein alpha, a negative regulator of macrophage phagocytosis allowing repression of rat macro

229 host defense mechanisms, including impairing macrophage phagocytosis.

230 Microglia and macrophages play a critical role in choroidal neovascula

231 l review the molecular mechanisms related to macrophage polarization and the interactions between sig

232 , the influence of protein ubiquitination on macrophage polarization has not been well studied.

233 -alpha, IL-6, and IL-1beta and in limited M1 macrophage polarization.

234 ative phosphorylation has been implicated in macrophage polarization.

235 thermogenesis in SAT, in part by slanting M2 macrophage polarization.

236 ventions modulate Kupffer cell activation or macrophage polarization.

237 In contrast, our data define a novel macrophage population that controls overwhelming inflamm

238 interest in how different dendritic cell and macrophage populations contribute to T cell-mediated imm

239 ferential polarization of ATMs, with M2-like macrophages predominant in lean AT and M1-like macrophag

240 additionally revealed that anti-inflammatory macrophages promoted HIF-associated vascularization and

241 for significantly higher levels of monocyte/macrophage proteins in SAGN-mainly lysozyme and S100A9.

242 We propose a model where macrophage recruitment to and activation at overgrowing

243 ion, increased B cell numbers, and decreased macrophage recruitment.

244 ckade following ablation enabled spontaneous macrophage regeneration, which fully restored original m

245 We show that apoptotic lymphocytes and macrophages release specific metabolites, while retainin

246 Most macrophages require colony-stimulating factor 1 receptor

247 However, a dysregulated macrophage response can be damaging to the host, as is s

248 subunit METTL14 in myeloid cells exacerbates macrophage responses to acute bacterial infection in mic

249 taining immune quiescence of tissue-resident macrophages, resulting in genetically programmed suscept

250 binds to its receptor on Leishmania-infected macrophages, resulting in their activation, production o

251 Splenic red pulp macrophages (RPMs) contribute to erythrocyte homeostasis

252 Loss of HDAC3 in macrophages safeguards mice from lethal exposure to lipo

253 are characterized by unorganized clusters of macrophages scattered between lymphocytes.

254 In conclusion, CD163-expressing macrophages serve as a protective mechanism to prevent t

255 provide a new resource for understanding how macrophages shape their proteome to meet the challenge o

256 mall interfering RNA studies in mice primary macrophages, showed that the transcriptional response do

257 also be enriched from post-ATI plasma using macrophage-specific (CD14) but not CD4+ T cell-specific

258 Mice harboring a macrophage-specific deletion of BCAP fail to recover fro

259 of the intima of lesions, here we identify a macrophage-specific lncRNA MAARS (Macrophage-Associated

260 s analyses of aortas of transgenic mice with macrophage-specific overexpression of urokinase (SR-uPA(

261 Vpr counteracts a previously unknown macrophage-specific restriction factor that targets and

262 rofiles are different among polarized murine macrophage subsets.

263 tose tumor cells, while anti-inflammatory M2 macrophages such as tumor-associated macrophages (TAMs)

264 Rather than producing cholesterol, microglia/macrophages synthesized desmosterol, the immediate chole

265 Here we show that macrophages take up HSV-1 via endocytosis and transport

266 lation of anti-inflammatory tumor-associated macrophages (TAM) is associated with worse clinical outc

267 tory M2 macrophages such as tumor-associated macrophages (TAMs) promote tumor growth and invasion.

268 blocks the proliferation of tumor associated macrophages (TAMs) through multiple mechanisms, partly b

269 microenvironment created by tumor-associated macrophages (TAMs).

270 ensated by gain of adjacent monocyte-derived macrophages that exhibited convergent epigenomes, transc

271 almitate up-regulates pannexin-1 channels in macrophages that mediate the attraction of neutrophils,

272 xcept for mast cells and nonmigratory CD163+ macrophages that were only present in biopsy isolates.

273 the ability of donor-derived resident renal macrophages to act as professional antigen-presenting ce

274 expression of Cxcl9l recruits mpeg1-positive macrophages to bone matrix and triggers their differenti

275 Environmental signals polarize macrophages to either a proinflammatory (M1) state or an

276 They suggest that targeting lung macrophages to increase their phagocytic capacity, enhan

277 territorial restriction of monocyte-derived macrophages to infarct tissue.

278 PTPN2 controls interactions between IECs and macrophages to maintain intestinal barrier function.

279 Exposing macrophages to purified SL-1 enhanced the trafficking of

280 y pamoic acid reprograms Ly-6C(Lo) monocytes/macrophages to relay a neuroprotective signal into the i

281 obactin under iron-stress conditions in host macrophages to support the iron demands of the pathogen.

282 Intralipid also promotes the polarization of macrophages to the anti-cancer M1-like phenotype.

283 al and clinical evidence support the role of macrophage Toll-like receptor signaling in maternal anti

284 e resulting MDK-modulated secretome educated macrophages towards tolerant phenotypes that promoted CD

285 here focuses on the ectopic presence of both macrophage types in the extracellular site surrounding t

286 nsor is applied to neuron-glial cultures and macrophage under the stimulation of lipopolysaccharide (

287 r the induction of these structures in mouse macrophages undergoing IL-4-mediated fusion.

288 complementation of infected WT and CSE(-/-) macrophages using the slow H(2)S releaser GYY3147 and th

289 At the implantation microenvironment, macrophages usually fuse into multinuclear cells, also k

290 mitive microglia and intracerebroventricular macrophages was eliminated, whereas the arrival of cepha

291 The precise locations occupied by pulmonary macrophages were defined in nondiseased human lungs from

292 CD163+ perivascular macrophages were identified by immunohistochemistry in b

293 in the spleen, suggesting that PnV-activated macrophages were led preferentially to the tumor.

294 on of stromal lamellae, with the presence of macrophages whose cytoplasm appeared clear and granular.

295 The interaction of dendritic cells and macrophages with a variety of rigid noncellular particle

296 In contrast, co-culture of LVS-infected macrophages with LVS-immune lymphocytes halted LVS repli

297 , we explored the function of this kinase in macrophages with studies of its regulation of the NLR fa

298 re susceptible to the degradative pathway of macrophages with upregulation of immunity relevant cytok

299 XR/RXR as the most enriched pathway in large macrophages, with up-regulation of genes involved in cho

300 ng myofibers and interstitial cells, such as macrophages, within muscle.