ライフサイエンスコーパス: macrophage cell

1 ndependent of protein expression within live macrophage cells.

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

3 suppresses production of bactericidal NO in macrophage cells.

4 fect the viral replication in swine alveolar macrophage cells.

5 ore as a fluorescent probe on the example of macrophage cells.

6 etion of mature IL-1beta (m-IL-1beta) in non-macrophage cells.

7 adhesive interactions between erythroid and macrophage cells.

8 gulation of necroptosis by cathepsins within macrophage cells.

9 glutathione-conjugated metabolite), against macrophage cells.

10 illumination microscopy (SIM) in J774 mouse macrophage cells.

11 ity index (SI) of 6.7 and no cytotoxicity to macrophage cells.

12 NA, protein, and promoter activity in murine macrophage cells.

13 evented LPS-mediated activation of Raw 264.7 macrophage cells.

14 owed for non-targeted, fluid-phase uptake by macrophage cells.

15 ent transcription from HIV-1 LTR in monocyte/macrophage cells.

16 mug/ml LPS exhibited no cytotoxic effects on macrophage cells.

17 mine the metabolic response of a 2D layer of macrophage cells.

18 e (LPS)-induced proinflammatory responses in macrophage cells.

19 ti-inflammatory activity on RAW 264.7 murine macrophage cells.

20 so demonstrated in the presence of RAW 264.7 macrophage cells.

21 osphate from small molecules present in host macrophage cells.

22 deacetylase-2 (HDAC2) in lung epithelial and macrophage cells.

23 iguing form of cell-to-cell transfer between macrophage cells.

24 mmatory cytokine production from human THP-1 macrophage cells.

25 ing activation of Kupffer cells and monocyte/macrophage cells.

26 tor 4 and STAT3-dependent mechanism in human macrophage cells.

27 onds of interaction of the bacteria with the macrophage cells.

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

29 stimulate cAMP increases in RAW264.7 murine macrophage cells.

30 f ER- associated miRNPs observed in infected macrophage cells.

31 potted fever, able to activate dendritic and macrophage cells.

32 pared with release in noncancerous RAW 264.7 macrophage cells.

33 correlating with TNFalpha secretion in mouse macrophage cells.

34 assessed in LPS-stimulated RAW 264.7 murine macrophage cells.

35 g intracellular MRSA present inside infected macrophage cells.

36 ) in lipopolysaccharide-stimulated RAW 264.7 macrophage cells.

37 uces the cytotoxicity of the chelator in the macrophage cells.

38 Understanding the interaction between macrophage cells and Bacillus anthracis spores is of sig

39 the detection of nitric oxide released from macrophage cells and endothelial cells, demonstrating th

40 lization of perfluorocarbon nanoemulsions in macrophage cells and for measurements of mechanical forc

41 les (Ag-MBA@SiO(2)) were taken up by J774A.1 macrophage cells and measured a decrease in local pH dur

42 ging of HOCl fluctuations produced in living macrophage cells and peritonitis of living mice with hig

43 In this study, we show that in both RAW264.7 macrophage cells and primary bone marrow-derived macroph

44 rate that MVs can be delivered into cultured macrophage cells and subsequently stimulate a potent IFN

45 PHs display superior cell penetration within macrophage cells, and in some cases, minimal cytotoxicit

46 diatom-biosilica is non-cytotoxic to J774.2 macrophage cells, and supports cell proliferation and gr

47 translocate the effector protein VgrG-1 into macrophage cells, and T6SS activation leads to fecal dia

48 expression level of IL-1beta in LPS induced macrophage cells, and to cause significant reduction of

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

50 ing LPS-induced proinflammatory responses in macrophage cells as well as in its interaction with LPS.

51 ble to inflict cellular damage in Caco-2 and macrophage cells, as assayed by LDH release, and escape

52 ld lower cytotoxicity toward RAW 264.7 mouse macrophage cells, as compared to the commercial transfec

53 -4 (IL-4) and IL-13 mediate their effects on macrophage cell biology, their biosynthesis, and respons

54 mulates C3 gene expression in human monocyte-macrophage cells but not in human hepatoma (HepG2) cells

55 ion of LPS-induced inflammatory responses in macrophage cells by melittin.

56 tigotes when transformed into amastigotes in macrophage cells cannot be cured by treatment of macroph

57 atory responses in RAW 264.7 murine monocyte/macrophage cells challenged with the TLR4 agonist LPS an

58 tected in the supernatants in VTRS1-infected macrophage cell culture.

59 F replicates as efficiently in primary swine macrophage cell cultures as the parental virus.

60 relation to atherosclerosis, using as model macrophage cell cultures enriched with LDL particles.

61 ory cytokine and chemokine programs in mouse macrophage cell cultures, along with depression of innat

62 as been well studied, processes that control macrophage cell death and HMGB1 release in animals are p

63 were defective in Yop-mediated inhibition of macrophage cell death and ROS production in neutrophil-l

64 crosis as the dominant mechanism of alveolar macrophage cell death in pneumococcal pneumonia.

65 Mycobacterium tuberculosis modulation of macrophage cell death is a well-documented phenomenon, b

66 nt a unique mechanism of MSU crystal-induced macrophage cell death not rescued by pan-cathepsin inhib

67 triggers in induction of Cer production and macrophage cell death through elevated expression of A-F

68 etwork analysis predicted that VTRS1-induced macrophage cell death was mediated by a proinflammatory

69 VTRS1-induced macrophage cell death was significantly inhibited by a c

70 TNF-alpha and IkappaB-alpha in VTRS1-induced macrophage cell death were further confirmed by individu

71 the role of A-FABP in promoting sFA-induced macrophage cell death with primary bone marrow-derived m

72 ent of the effects of IFN-beta on ST-induced macrophage cell death, but significantly dependent on IL

73 red for non-canonical inflammasome-triggered macrophage cell death, indicating that caspase-11 orches

74 r investigate the mechanism of VTRS1-induced macrophage cell death, microarrays were used to analyze

75 -8 and the RIP kinases are key regulators of macrophage cell death, NF-kappaB and inflammasome activa

76 RC4 causes constitutive IL1FC production and macrophage cell death.

77 ted heme-induced oxidative burst and blocked macrophage cell death.

78 n VTRS1 (a vaccine candidate) induced strong macrophage cell death.

79 lammatory, caspase-2- and NF-kappaB-mediated macrophage cell death.

80 ted FAs (sFAs), are able to directly trigger macrophage cell death.

81 ar potassium stores could avoid HlyA induced macrophage cell death.

82 ppressing IFN-gamma-mediated monocyte and/or macrophage cell death.

83 pha production induced by LPS stimulation in macrophage cells differentiated from THP-1 cells.

84 stimulation, NR4A receptor-depleted monocyte/macrophage cells display significantly altered expressio

85 While we investigate ILM macrophage cells distinct from the larger sample of over

86 aging, we found reduced numbers of alveolar macrophages, cells essential for lung homeostasis.

87 In RAW 264.7 macrophage cells, expressed Arf6-GFP partially colocaliz

88 -4 signaling pathways that are important for macrophage cell fate choice.

89 of microenvironmental signals that determine macrophage cell fate decisions to establish appropriate

90 myelination, tumor suppression, and monocyte/macrophage cell fate determination.

91 usands of myeloid enhancers in a monocyte-to-macrophage cell fate model.

92 test were conducted on J774A.1 cells murine macrophage cells for different glass concentrations.

93 phase binding assay, and it protected murine macrophage cells from intoxication with LT.

94 However, bone marrow macrophage cells from MAGP1Delta mice show a higher prop

95 ts showed that in B10.S, SJL/J, and RAW264.7 macrophage cells, IL-6 expression was dependent on extra

96 of THP stimulated the proliferation of human macrophage cells in culture and partially restored the n

97 sembly can influence their interactions with macrophage cells in culture.

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

99 2 and IL-6) clustering with CD68(+) monocyte/macrophage cells in livers of subjects with dAIH, and is

100 was correlated with an increase in alveolar macrophage cells in the lungs and airways, early inducti

101 atory cytokines in RAW 264.7 and rat primary macrophage cells in the presence of LPS, MM-2 and Mel-SC

102 shapes, and (4) are efficiently taken up by macrophage cells in vitro.

103 lpha in mouse bone marrow cells and monocyte/macrophage cells, in the absence of receptor activator o

104 ell metabolomic profiling using rat alveolar macrophage cells incubated with different concentrations

105 em to separate interaction stages and single macrophage cells infected with C. albicans from uninfect

106 that the inflammasome was not activated upon macrophage cell infection with murine gammaherpesvirus 6

107 fiber central nucleation and increased focal macrophage cell infiltration, indicating exacerbated dys

108 eoclasts derived from MAGP1Delta bone marrow macrophage cells is increased relative to the wild type,

109 from a dendritic cell line (JAWS II), from a macrophage cell line (C2.3), and from murine primary bon

110 thout affecting potassium efflux, in a mouse macrophage cell line (J774), mouse bone marrow-derived d

111 uced the signal transduction in chicken HD11 macrophage cell line (p < 0.05).

112 the sequenced strain, PAO1, toward a murine macrophage cell line (RAW 264.7).

113 f cell migration response, particularly in a macrophage cell line (RAW/LR5) and only modestly in the

114 tivators as well as NFkappaB activation in a macrophage cell line (RAW264.7); however, DOPG was not i

115 d monocyte chemotactic protein-1 in a murine macrophage cell line and human primary macrophages.

116 by DNA affinity isolation from the RAW264.7 macrophage cell line and identified by mass spectrometry

117 tify genes overexpressed in the HD11 chicken macrophage cell line and in primary chicken oviduct epit

118 mediators induced autophagy in the RAW246.7 macrophage cell line and in primary monocytes.

119 propose that exposure of macrophages (both a macrophage cell line and primary human alveolar macropha

120 nt debris both in vitro (using a human THP-1 macrophage cell line and primary human monocytes/macroph

121 induced IL-27 mRNA and protein levels in the macrophage cell line and primary lung monocytes/macropha

122 nducing secretion of TNF-alpha by a monocyte/macrophage cell line and primary macrophages.

123 llular bacterial killing by a mouse alveolar macrophage cell line and primary mouse neutrophils.

124 ein activates cytokine production in a human macrophage cell line as well.

125 Chlamydia muridarum in the RAW 264.7 murine macrophage cell line at different MOIs.

126 ty similar to their mammalian orthologs in a macrophage cell line bioassay.

127 hepatic macrophages (HMacs) and in a murine macrophage cell line by coupling transcriptional upregul

128 e responses to lipopolysaccharide in a human macrophage cell line cultured in 86 mM ethanol, 1 mM ace

129 ed with this aberrant translation in MEFs, a macrophage cell line depleted of CPEB and treated with l

130 We also show that the J774.2 macrophage cell line exhibits unusual intracellular upta

131 A macrophage cell line expressing Dectin-1 was employed to

132 The fragments were cultured with RAW 264.7 macrophage cell line for 9 weeks.

133 modulate the immune response in the chicken macrophage cell line HD11 and in chicken primary monocyt

134 tively high in the thymus and in the chicken macrophage cell line HD11.

135 computed tomography imaging in the RAW 264.7 macrophage cell line identified the formulation that pro

136 We found that supernatants of a human macrophage cell line infected with either of the bacteri

137 Overexpression of SLAT in a macrophage cell line inhibits the IgG Fcgamma receptor-m

138 Hca2 expression in the RAW264.7 murine macrophage cell line is strongly induced by LPS treatmen

139 ROS production was measured in the murine macrophage cell line J774 and in primary phagocytes usin

140 otic stress and killing by the mouse-derived macrophage cell line J774.

141 ns were toxic to mammalian cells, the murine macrophage cell line J774.16, in a LLO-dependent manner,

142 r knockdown of Aim2 expression in the murine macrophage cell line J774.A1, IFN-beta treatment of cell

143 reduced cytokine production in the alveolar macrophage cell line MH-S.

144 Moreover, macrophage cell line models RAW264.7 and THP-1, as well

145 Knockdown of Nab1 in a macrophage cell line prevented downregulation of IFNGR1

146 from M-JAK2(-/-) mice and Jak2 knockdown in macrophage cell line RAW 264.7 also showed lower levels

147 We also observed MET formation by the mouse macrophage cell line RAW 264.7 and by human THP-1 cell-d

148 We used macrophage cell line RAW 264.7 and human embryonic kidne

149 induced tolerant cells; knockdown of Neu1 in macrophage cell line RAW 264.7 cells resulted in enhance

150 In vitro, stable knockdown of HuR in mouse macrophage cell line RAW 264.7 corroborated in vivo data

151 The murine macrophage cell line RAW 264.7 was three-dimensionally c

152 The mouse macrophage cell line Raw 264.7, mouse primary lung monoc

153 se colon carcinoma cell line MC38, the mouse macrophage cell line RAW 264.7, or mouse and human organ

154 te-derived macrophages (MDMs) and the murine macrophage cell line RAW 264.7.

155 s effect on pro-inflammatory activity in the macrophage cell line RAW 264.7.

156 y, p66Shc was knocked down with siRNA in the macrophage cell line RAW264, and a 30% defect in superox

157 Similar results were obtained in the mouse macrophage cell line RAW264.7 after LPS treatment.

158 t on the inflammatory response of the murine macrophage cell line RAW264.7 and human monocyte THP-1 t

159 rmined that exosome production by the murine macrophage cell line RAW264.7 requires the endosomal sor

160 alveolar and peritoneal macrophages and the macrophage cell line RAW264.7, but not in primary bone m

161 hibition of dysferlin expression in the J774 macrophage cell line resulted in significantly enhanced

162 Overexpression of gga-miR-429 in the HD11 macrophage cell line significantly inhibited TMEFF2 and

163 Similar results were obtained in a murine macrophage cell line stimulated with the TLR7 agonist co

164 (B6.Nba2-ABC) splenic cells and in a murine macrophage cell line that overexpressed p202 protein was

165 This effect was also observed in the macrophage cell line THP-1.

166 ival in primary murine macrophages and human macrophage cell line THP-1.

167 Use of a macrophage cell line to evaluate cytotoxic and ROS produ

168 derived from CD44-deficient mice, in an MH-S macrophage cell line treated with antibodies to CD44, or

169 Conversely, the AM macrophage cell line was more responsive to P. gingivali

170 Specifically, using the RAW 264.7 mouse macrophage cell line we show that whole OSPW containing

171 man monocyte-derived macrophages and a mouse macrophage cell line were used to determine effects of c

172 Coculturing a macrophage cell line with hypoxia-treated primary tubule

173 34Delta cells after phagocytosis by a murine macrophage cell line, and Atg8 expression was exhibited

174 J2-C8 cell line (AM cells), a mouse alveolar macrophage cell line, and ESK-1 cells, a mouse gingival

175 restingly, sCD16 inhibited MDALDL binding to macrophage cell line, as well as soluble forms of recomb

176 genesis of RAW264.7 cells, a murine monocyte/macrophage cell line, by suppressing the induction of NF

177 Our results show that in an alveolar macrophage cell line, cellular ROS responses are highly

178 of SCN8A from THP-1 cells, a human monocyte-macrophage cell line, confirmed the expression of a full

179 of IL-12p40 was investigated using a murine macrophage cell line, CRL2019, in an in vitro MW model.

180 Ocm), a Ca(2+)-binding protein secreted by a macrophage cell line, is a potent axon-promoting factor

181 cells in the presence of an irradiated mouse macrophage cell line, J774A.1.

182 e showed that in primary keratinocytes and a macrophage cell line, PG suppressed inflammatory mediato

183 Similarly, treatment of human PBMCs or mouse macrophage cell line, RAW 264.4, with TGF-beta, induced

184 In mouse macrophage cell line, RAW264.7, while both BLP and LPS s

185 In a macrophage cell line, regulation of IL-10 by BAR501 was

186 In vitro in a human macrophage cell line, SLM (10(-8) mol/L) enhanced FP (10

187 Using a mouse macrophage cell line, this report studied the impact of

188 Employing a rat alveolar macrophage cell line, we found that exposure to silica d

189 Using a murine macrophage cell line, we showed that the F. nucleatum-in

190 optimize uptake conditions in the RAW 264.7 macrophage cell line.

191 proteome during infection of a human-derived macrophage cell line.

192 nd c-Maf expression in microglia and the RAW macrophage cell line.

193 aB production upon light exposure in a model macrophage cell line.

194 efflux, such as Abca1, Abcg1, and Apoe, in a macrophage cell line.

195 ability to grow in mouse serum and a J774.16 macrophage cell line.

196 A ablation of C/EBPbeta in a murine alveolar macrophage cell line.

197 lood, spleen, and bone marrow and from a rat macrophage cell line.

198 th IL-36alpha activated NF-kappaB in a mouse macrophage cell line.

199 m and efficiency of nanoparticle uptake by a macrophage cell line.

200 e 50 promoter represses activity in a murine macrophage cell line.

201 ow-density lipoprotein (oxLDL) by a monocyte/macrophage cell line.

202 or poly(I:C), a TLR3 agonist in the RAW264.7 macrophage cell line.

203 phagocytosed Escherichia coli in a cultured macrophage cell line.

204 ts the LPS effect using a PMJ2-PC peritoneal macrophage cell line.

205 oxygenase, no cytotoxicity against RAW 264.7 macrophage cells line, and a weak potential to decrease

206 targeting of FXIII-A in the THP-1 (monocyte/macrophage) cell line and in human monocyte-derived macr

207 cessfully detected at therapeutic dosages in macrophages (cell line: NR8383).

208 Endothelial cells (cell line: TIME) and macrophages (cell line: RAW264.7) were treated with vari

209 Overexpression of NNT in a macrophage cell-line resulted in decreased levels of rea

210 o be upregulated in M. leprae-infected human macrophage cell lineages, primary monocytes, and skin le

211 The ability of 2 macrophage cell lines (HL-60; RAW 264.7) to kill archety

212 ages (C57BL/6, BALB/c, and p47(phox-/-)) and macrophage cell lines (RAW 264.7 and IC21) to investigat

213 ndirectly promoted the uptake of bacteria by macrophage cell lines and directly killed bacteria at ac

214 In vitro studies were performed in macrophage cell lines and in isolated mouse macrophages

215 ependent manner in human and murine monocyte/macrophage cell lines and in primary macrophages.

216 ver, the mutant shows impaired growth within macrophage cell lines and is severely attenuated in zebr

217 er into both folate receptor beta-expressing macrophage cell lines and primary mouse macrophages.

218 for survival/growth within human and murine macrophage cell lines and was unable to escape from phag

219 Inhibition or deficiency of A-FABP in macrophage cell lines decreased sFA-induced Cer producti

220 ated in a time- and dose-dependent manner in macrophage cell lines derived from AFABP/aP2-EFABP/mal1

221 Interestingly, not all mouse macrophage cell lines permit GP-F88A entry.

222 Studies with RAW264.7 and J774 macrophage cell lines reveal that Dragon negatively regu

223 Invasion assays using epithelial and macrophage cell lines revealed differences in the abilit

224 Fibroblast and macrophage cell lines shared a cluster of such "NF-kappa

225 e we show, with global proteomic analysis of macrophage cell lines treated with either IFNgamma or IL

226 fect different primary cells and established macrophage cell lines with deletions in the Toll-like re

227 ilitate such virulence screens, we developed macrophage cell lines with which the number of intact ho

228 thogen to inhibit the phagocytic activity of macrophage cell lines, an event that can be correlated w

229 GILZ was inducible by curcumin in macrophage cell lines, primary human monocyte-derived ma

230 ing to stably knock out and recover Rab8a in macrophage cell lines, we match Akt signaling profiles w

231 human mammary epithelial cells and monocyte/macrophage cell lines, we show that the chromatin bounda

232 2(-/-) and TLR4(-/-) than in wild type mouse macrophage cell lines.

233 shed in murine MS1 endothelial and RAW 264.7 macrophage cell lines.

234 on of the HSV-1 DNA genome in differentiated macrophage cell lines.

235 uman epithelial, mouse fibroblast, and mouse macrophage cell lines.

236 ibodies to oxLDL (oxLDL-IC) in monocytic and macrophage cell lines.

237 production of cytotoxic ceramides (Cers) in macrophage cell lines.

238 ndent intracellular growth of B. neotomae in macrophage cell lines.

239 we used primary hepatocytes and hepatoma and macrophage cell lines.

240 T12 (mouse fibroblast), and RAW 264.7 (mouse macrophage) cell lines.

241 ngs, CCR7 gene expression in human and mouse macrophages cell lines is induced when LXRalpha at S198

242 An in vitro assay on macrophage cell lysates showed complete inhibition of SP

243 rong inhibition of SPSB2-iNOS interaction in macrophage cell lysates.

244 Our findings indicate that human ILM macrophage cells may be distributed distinctly, age diff

245 upregulation occurs in many human and murine macrophage cell models and also primary cells.

246 esulted in significant reduction in monocyte/macrophage cell numbers within PBMCs in a dose-dependent

247 Stealth microrobots avoid detection by macrophage cells of the innate immune system after exhau

248 g vertebrates, was downregulated in RAW264.7 macrophage cells of the M2 phenotype in conditoned mediu

249 Using RAW 264.7 macrophage cells or 3T3-L1 adipocytes, C/EBPbeta knockdo

250 NADPH fluctuations during the activation of macrophage cells or wound response in vivo.

251 21R system should consider that monocyte and macrophage cell physiology may be affected by this syste

252 ed increased levels of DPP4 expression in DC/macrophage cell populations from visceral adipose tissue

253 It selectively visualized monocyte and macrophage cell populations in vitro, by live-cell imagi

254 00-500 nm was demonstrated by stimulation of macrophage cell proliferation.

255 sed on interference with FcgammaR-stimulated macrophage cell proliferation.

256 This sensor was integrated within mouse macrophage cells (RAW 264.7) with multiple serotypes of

257 popolysaccharide (LPS) stimulation of murine macrophage cells (RAW 264.7).

258 Peripheral macrophage cells responded to rod cell loss, as evidence

259 siRNA or functional TR4 cDNA in the RAW264.7 macrophage cells resulted in either decreased or increas

260 ng functional CD36 cDNA in the TR4 knockdown macrophage cells reversed the decreased foam cell format

261 pressures in either epithelial, neuronal, or macrophage cells reverted to WT sequence.

262 Using a micropatterning approach to control macrophage cell shape directly, we demonstrate here that

263 lzheimer's disease are enriched in different macrophage cell states.

264 eritoneal macrophages, we confirm a role for macrophage cell surface beta3 integrin in this dl922-947

265 Neutralization of RA synovial fluid macrophage cell surface gp96 inhibited the constitutive

266 erized by expression of both DC and monocyte/macrophage cell surface markers.

267 We demonstrate the utility of these macrophage cell systems for siRNA screening of pathogen

268 epresent one of the frequently used monocyte/macrophage cell systems to study immune responses.

269 s approach by imaging human monocyte-derived macrophage cells that have been exposed to fibrils from

270 we hypothesize that the removal of the liver macrophages, cells that have been reported to take up th

271 based on the study of blood monocyte-derived macrophages, cells that have never been exposed to the w

272 Macrophage cell therapy improves clinically relevant par

273 d the emergence of chimeric antigen receptor macrophage cell therapy.

274 Nfatc1, and Ctsk, and it reprograms monocyte/macrophage cells to OC-like cells.

275 asma virulence, we employed these transgenic macrophage cells to screen a collection of individual tr

276 We propose that macrophage cell-to-cell transfer represents a nonlytic e

277 gas phase and fluorescence imaging of NO2 in macrophage cells treated with a nitrogen dioxide donor.

278 crease in the optical force was also seen in macrophage cells treated with cytochalasin D, both with

279 xpressed JunB is cleaved in murine RAW 264.7 macrophage cells treated with the NALP1b inflammasome ac

280 the stress pathways activated, depending on macrophage cell type, consistent with the nonspecific na

281 onfirmed in vivo in mice with hepatocyte and macrophage cell-type-specific conditional Ron deletions.

282 us NO cytotoxicity in two well characterized macrophage cell types (J774 and RAW 264.7).

283 that overexpress AOAH in dendritic cells and macrophages, cell types that normally produce it.

284 s, the aggregates are stable and nontoxic to macrophage cells up to 55 x 10(-3) m Au.

285 in the optical force experienced by RAW264.7 macrophage cells upon the uptake of both microparticles

286 ied particles remained resistant to cultured macrophage cell uptake, although they were still quickly

287 The infiltration of polymorphonuclear and macrophage cells was associated with increased ocular me

288 lipopolysaccharide (LPS)-stimulated J774A.1 macrophage cells was investigated.

289 e viability and ATP levels in epithelial and macrophage cells, we discovered for fumed silica an impo

290 Applied to complex macrophage cells, we extract the quantification of major

291 of the first indicators of oxidative burst, macrophage cells were exposed within the microfluidic de

292 Dendritic and macrophage cells were found to be important for this cro

293 ession analysis of bacteria infecting murine macrophage cells were performed under four distinct cond

294 RAW264.7 mouse macrophage cells were pretreated with phenylmethimazole

295 Finally, macrophage cells were treated with two selected nanopart

296 e latter case by taking PSFC measurements of macrophage cells when inoculated with enhanced green flu

297 sc1), is required for fungal survival inside macrophage cells, which is consistent with the role of F

298 Further, transfection of RAW264.7 macrophage cells with the miR-19a-3p mimic decreased the

299 Microglia, the resident macrophage cells within the central nervous system (CNS)

300 retinal microglia, the ability to visualize macrophage cells without fluorescent labeling in the liv