ライフサイエンスコーパス: monocytic

1 dhesion molecule-1 expression to increase EC-monocytic adhesion, but the Ser45/Thr41-phosphorylated b

2 ling pathways, leading to myelomonocytic and monocytic AML cell differentiation.

3 therapeutic potential in myelomonocytic and monocytic AMLs.

4 Ccr2, Ccr3, and Ccr5, which together control monocytic and eosinophilic recruitment to resting and in

5 ased early type I IFN transcription in human monocytic and epithelial cell lines, but this was surpri

6 possibly via interacting with NLRC3 in human monocytic and epithelial cells.

7 Of the expanded monocytic and granulocytic cell populations of MDSCs, th

8 aused by excessive proliferation of cells of monocytic and granulocytic lineages.

9 These cell subsets include monocytic and granulocytic myeloid-derived suppressor ce

10 CXCR3 is associated with monocytic and lymphocytic infiltration of inflamed or tu

11 block in T-lineage specification and induced monocytic and plasmacytoid dendritic cell differentiatio

12 MDSCs consist of two major subsets, monocytic and polymorphonuclear (PMN).

13 Application of LPHAMS to U937 monocytic and primary murine and human endothelial cells

14 Human monocytic and professional antigen-presenting cells have

15 lved in activating HIV-1 by I-BET151 in both monocytic and T cells, CDK2 enhanced HIV-1 transcription

16 dividuals, were found to express epithelial, monocytic, and endothelial protein markers and were obse

17 ne differentiation trajectories of vascular, monocytic, and fibroblastic lineages over regeneration,

18 The cellular response was predominantly monocytic, and focal fibroplasia was observed at the air

19 ensable for the development of granulocytic, monocytic, and megakaryocytic cells.

20 h clonally determined lymphoid, neutrophilic/monocytic, and/or erythroid progeny outputs from >1000 i

21 human sera markedly enhanced the capacity of monocytic APC to stimulate MAIT cells.

22 letion of common lymphoid progenitors, and a monocytic bias in comparison with the granulocytic bias

23 to polymorphonuclear (CADO48A(+)CD14(-)) and monocytic (CADO48A(-)CD14(+)) MDSC subsets.

24 granulocytic (CD11b(+)Ly6G(+)Ly6C(low)) and monocytic (CD11b(+)Ly6G(-)Ly6C(high)) myeloid-derived su

25 PRRSV is ideal for deciphering how monocytic cell activation statuses interact with antivir

26 sisting after the infection resolves, and is monocytic cell dependent.

27 s relayed by the MKK6-p38MAPK cascade induce monocytic cell differentiation from band-stage neutrophi

28 Monocytic cell differentiation potential was retained in

29 C/EBPalpha, which enabled the induction of a monocytic cell differentiation program.

30 to induce inflammatory responses in a human monocytic cell line (THP-1 cells).

31 ecretion were conducted with the human THP-1 monocytic cell line and corroborated in primary human pe

32 we knocked down these proteins in the human monocytic cell line Mono Mac 6 (MM6).

33 of the pro-inflammatory cytokine IL-6 in the monocytic cell line Mono Mac 6, induction of the Toll-in

34 e resulting products against the THP-1 human monocytic cell line revealed hitherto unrecognized trend

35 y, we observe that depletion of BICD2 in the monocytic cell line THP-1 results in an induction of IFN

36 nhibited CCL2-driven chemotaxis of the human monocytic cell line THP-1, CCL3-driven chemotaxis of per

37 vity in a time-dependent manner in the human monocytic cell line THP1.

38 trophils and diminished calcium signaling in monocytic cell line U937 transfected with the C5a recept

39 A human monocytic cell line was genetically engineered using len

40 Knocking down DJ-1 (siRNA) in THP-1 (human monocytic cell line) and polymorphonuclear cells from pa

41 mooth muscle cells and THP-1 (human leukemia monocytic cell line) macrophages stimulated with lipopol

42 We used a human monocytic cell line, THP-1, and dendritic cells to study

43 man airway smooth muscle cells and the human monocytic cell line, THP-1.

44 ester accumulation in foam cells of the THP1 monocytic cell line.

45 ased consequent late cell death of the human monocytic cell line.

46 transcription in microglial cells (HC69) and monocytic cell lines (U1 and OM10.1).

47 nse to various inflammatory stimuli in human monocytic cell lines and murine bone marrow-derived macr

48 induces less inflammatory signaling in human monocytic cell lines and murine macrophages than the par

49 vatives of the A549 lung carcinoma and THP-1 monocytic cell lines and used these to study T cell resp

50 cycle in primary human T lymphocytes and in monocytic cell lines.

51 e suppression of HIV in human microglial and monocytic cell lines.

52 se receptors in establishing tissue-resident monocytic cell populations.

53 We observed spontaneous monocytic-cell infiltration in the lungs of Serpine2-def

54 g various phases of HIV-1 infection using U1 monocytic cells (latently infected U937 cells with HIV-1

55 human epithelial pulmonary cells (A549) and monocytic cells (U937) upon IAV infection using synchrot

56 FXa) activity by IgG-containing ICs by THP-1 monocytic cells and human monocytes.

57 HoloBLG shuttled iron into monocytic cells and impaired their antigen presentation.

58 s (PRRSV), which directly infects subsets of monocytic cells and interferes with antiviral responses.

59 (Gal3), a pleiotropic lectin, is produced by monocytic cells and macrophages.

60 vivo activated HIV-1 gene expression only in monocytic cells and not in CD4(+) T cells.

61 We treated human THP-1 monocytic cells and primary human blood monocytes with R

62 nity, because it directly infects subsets of monocytic cells and subverts overall immune responses.

63 jacked" leukocytes, previously identified as monocytic cells and T lymphocytes, transmit EHV1 to endo

64 Importantly, porcine monocytic cells at different activation states were susc

65 se pathways in uninfected and PRRSV-infected monocytic cells at different activation states.

66 Although it induces chemotaxis of monocytic cells at high concentrations, its physiologica

67 cells, CDK2 enhanced HIV-1 transcription in monocytic cells but inhibited it in T cells.

68 We observed that monocytic cells cocultured (but not in contact) with ECs

69 els of CYP2E1 caused significant toxicity in monocytic cells compared to exosomes derived from contro

70 A forms and induced less TNF-alpha in THP-1 monocytic cells compared with LOS from group 1.

71 se of the autofluorescent signal recorded in monocytic cells could be correlated with the IR detectio

72 ytic cells with nonrespiring mitochondria or monocytic cells cultured in the presence of pyruvate or

73 fect of Panx1 deletion in endothelial and/or monocytic cells during atherogenesis is counterbalanced

74 respiratory epithelial cells and circulating monocytic cells efficiently transferred virions to T lym

75 In particular, miR-10a was transferred to monocytic cells from EC-EVs and could repress inflammato

76 Monocytic cells have been found to be an important part

77 us cellular ecosystems, where non-neoplastic monocytic cells have emerged as key regulators of tumor

78 nsfusion of haematopoietic-stem-cell-derived monocytic cells in newborn mice is sufficient to rescue

79 r, our study reveals a dynamic modulation of monocytic cells in response to varying dosages of endoto

80 ecreted by primary human monocytes and THP-1 monocytic cells in the presence of alcohol in a concentr

81 in the gastrointestinal tract) and lymphoid/monocytic cells in tonsils and Peyer's patches (explaini

82 in the gastrointestinal tract) and lymphoid/monocytic cells in tonsils and Peyer's patches (explaini

83 ctures in the ECM, providing a substrate for monocytic cells in vitro, whereas lung fibroblasts from

84 We showed that in monocytic cells KLF4 has to be repressed to allow their

85 uence of HIV on global lncRNAs expression in monocytic cells lines.

86 ntiviral infection with activation status of monocytic cells may provide a means of potentiating anti

87 port that STAT3 is activated in infiltrating monocytic cells near active MS lesions and that activati

88 ured by flow cytometry using uptake by THP-1 monocytic cells of fluorescent beads coated with gp120,

89 ortunately, the activation status of porcine monocytic cells or how cell activation status functional

90 Monocytic cells perform crucial homeostatic and defensiv

91 erentially enhanced HIV-1 gene expression in monocytic cells rather than in T cells and that whereas

92 LPS (lipopolysaccharide)-stimulated monocytic cells release free mitochondria and microvesic

93 These monocytic cells represent one of the best-defined human

94 a consequence, parabiosis or transfusion of monocytic cells results in long-term gene transfer in os

95 f infected human, primary, neuronal stem and monocytic cells revealed effects on neurodevelopment and

96 s expression of APOL1 in differentiated U937 monocytic cells stimulated with IFN-gamma resulted in a

97 ) greater opsonization of these IEs by human monocytic cells than IgGs from malaria-exposed Malian me

98 linically characterized by overproduction of monocytic cells that can infiltrate organs, including th

99 olar and interstitial macrophages as well as monocytic cells that survey lung tissues.

100 ocaine treatment increased transmigration of monocytic cells through the HBMEC barrier.

101 aneous psoriatic lesions, and BMP7 instructs monocytic cells to acquire characteristics of psoriasis-

102 , we showed that Slit2 inhibited adhesion of monocytic cells to activated human endothelial cells, as

103 cs approach to assess the responses of human monocytic cells to Au-NPs of two different sizes with th

104 investigate the activation status of porcine monocytic cells to determine the intricate interaction o

105 nfluence the antigen presenting phenotype of monocytic cells to determine the nature of T cell respon

106 nt lipid mediators that activate THP-1 human monocytic cells to generate tumor necrosis factor alpha

107 aB epigenetically reprograms the response of monocytic cells to IFNgamma toward an immunosuppressive

108 tease thrombin in regulating the adhesion of monocytic cells to smooth muscle cells producing an infl

109 n and the recruitment of bone marrow-derived monocytic cells to the hypothalamus; in addition, this i

110 rom CD11c(dim)CD11b(int)Gr1(-) lung-resident monocytic cells transformed by KRAS(G12D) In contrast, B

111 ion-channel function of ATP receptor P2X7 in monocytic cells via nAChR containing alpha9 and alpha10

112 Inflammatory monocytic cells were not observed infiltrating the skin

113 nvolve iterative fusion of circulating blood monocytic cells with long-lived osteoclast syncytia.

114 stically reduced when they were derived from monocytic cells with nonrespiring mitochondria or monocy

115 luble CD163 likely originates from activated monocytic cells, as serum from stroke patients stimulate

116 and microvesicles released by LPS-activated monocytic cells, as well as circulating microvesicles is

117 describe a regulation of Dicer expression in monocytic cells, based on proteolysis.

118 ces the cytotoxicity of paclitaxel for human monocytic cells, but not for breast, lung, or pancreatic

119 ntially reactivated HIV-1 gene expression in monocytic cells, but not in CD4 T cells, in cART-treated

120 gnificantly increased HIV-1 transcription in monocytic cells, but not in HIV-1-infected CD4 T cells,

121 Monocytic cells, including macrophages and dendritic cel

122 Activation statuses of monocytic cells, including monocytes, macrophages (Mvarp

123 study antiviral responses in PRRSV-infected monocytic cells, we characterized inflammatory cytokine

124 ll types, primary human CD4 T-cells and U937 monocytic cells, were used to compare differences in cyt

125 rst genome-wide analysis of TNF tolerance in monocytic cells, which differentially inhibits NF-kappaB

126 occurs indirectly by mediators released from monocytic cells.

127 of innate immune responses in differentiated monocytic cells.

128 tective role for Panx1 in endothelial and/or monocytic cells.

129 yristate acetate (PMA) activated THP-1 human monocytic cells.

130 mpaired nuclear import of HIV-1 DNA in human monocytic cells.

131 atory host cells such as T cells and myeloid/monocytic cells.

132 ot contribute to IL-1beta release from human monocytic cells.

133 t to the secretome and the proteome of human monocytic cells.

134 ection with the activation status of porcine monocytic cells.

135 ge conversion from band-stage neutrophils to monocytic cells.

136 their effect on ALC/APAP-induced toxicity in monocytic cells.

137 nd APAP-induced toxicity in both hepatic and monocytic cells.

138 n gingival fibroblasts (HGFs) and U937 human monocytic cells; however, the responsible mechanisms hav

139 We treated hepatic and extra-hepatic (monocytic) cells with exosomes +/- ALC/APAP.

140 Hemangioblastic and monocytic cEPC levels were not correlated (Spearman corr

141 nvestigate the levels of hemangioblastic and monocytic cEPCs in patients with periodontitis and perio

142 A non-significant trend for higher levels of monocytic cEPCs in periodontitis was also observed.

143 sed untreated SLE patients shared a distinct monocytic chemokine signature, despite clinical heteroge

144 id not alter tumor incidence implicating the monocytic compartment as the functionally immunosuppress

145 C/EBPbeta deficiency favors the expansion of monocytic-derived DCs.

146 uman AML cases exhibited reduced morphologic monocytic differentiation and inferior survival.

147 erestingly, we discovered that KLF4-mediated monocytic differentiation is selectively dependent on on

148 thus yielding progenitors with a predominant monocytic differentiation potential.

149 clarify the molecular basis of KLF4-mediated monocytic differentiation, we performed detailed genetic

150 er a vascularized microenvironment promoting monocytic differentiation, while depleting leukemia-asso

151 Human monocytic ehrlichiosis (HME) is caused by a tick-borne o

152 ia chaffeensis, the etiologic agent of human monocytic ehrlichiosis (HME), has been extensively studi

153 ve intracellular bacterium that causes human monocytic ehrlichiosis (HME): a febrile illness that may

154 r tick-borne bacterium responsible for human monocytic ehrlichiosis.

155 ckettsial organism, causes the disease human monocytic ehrlichiosis.

156 ntracellular rickettsial agent, causes human monocytic ehrlichiosis.

157 -term rEC-hMPP-derived myeloid (granulocytic/monocytic, erythroid, megakaryocytic) and lymphoid (natu

158 Thus, IRF8 does not regulate granulocytic vs monocytic fate in GMPs, but instead acts downstream of l

159 ngiotensin-II infusion induced the uptake of monocytic fibroblast precursors that initiated the devel

160 inding assays demonstrated that granulocytic/monocytic (G/M) commitment is marked by Runx1 suppressio

161 uggest that BETi can preferentially activate monocytic HIV-1 reservoir cells and that a combination o

162 modulated the size and permissiveness of the monocytic host cell reservoir via regulation of IFN-gamm

163 ingle cell transcriptional profiles of THP-1 monocytic human leukemia cells.

164 o determine whether women with TMD exhibit a monocytic hyperinflammatory response compared with contr

165 res reduced iNKT proliferation and abrogated monocytic IL-12 production.

166 ments and Main Results: Peripheral blood and monocytic IL-18 expression escaped LPS-induced immunopar

167 om the resident microglia, we found that the monocytic infiltrates gradually adopted a ramified morph

168 CR2 chemoattractant pathway markedly reduced monocytic infiltrates, perineuronal nets, and autistic-l

169 istic effects in inducing neuroinflammation, monocytic infiltrates, synaptic defects, and perineurona

170 lammatory disease with characteristic lympho-monocytic infiltration in lungs, livers, and kidneys, al

171 lial N-glycosylation may impact vascular and monocytic inflammation.

172 ontrol women, and to examine associations of monocytic inflammatory responses with clinical pain.

173 hly susceptible to OPC, indicating that this monocytic influx is insufficient for host defense.

174 y, genetic or pharmacological obstruction of monocytic influx significantly reduced perineuronal net-

175 In the YS, EMPs gave rise to MFs without monocytic intermediates, while EMP seeding the FL upon t

176 oids was further evaluated using THP-1 human monocytic leukemia cell line.

177 Human fetal RPE and monocytic leukemia macrophage (THP-1) cell lines were cu

178 l lines, and on neoplastic cell lines: acute monocytic leukemia THP-1 and lung adenocarcinoma A549.

179 Here, we use deletion of the monocytic leukemia zinc finger gene (Moz/Kat6a/Myst3) to

180 FK activity was linked to recruitment of the monocytic leukemia zinc finger protein (MOZ) histone ace

181 Using stage-specific deletion of monocytic leukemia zinc finger protein (MOZ), a histone

182 ransferase complexes, where the gene of MOZ (monocytic leukemia zinc finger protein) was first identi

183 The monocytic leukemic zinc finger (MOZ) histone acetyltrans

184 s in the spleen that phenotypically resemble monocytic-like (CD11b(+)Ly6C(high)) and granulocytic-lik

185 megakaryocytic-erythroid versus granulocytic-monocytic lineage decision-making.

186 s), multinucleated giant cells (MGCs) of the monocytic lineage, is bone resorption.

187 absence of TLR4, IFN-gamma, or depletion of monocytic-lineage cells or CLEC-2 on platelets markedly

188 est the in vivo relevance of these findings, monocytic-lineage-specific GCN2KO mice were challenged w

189 to megakaryocytic-erythroid and granulocytic-monocytic lineages.

190 e-stage vaccine testing, we demonstrate that monocytic (M)-MDSCs and polymorphonuclear (PMN)-MDSCs ca

191 e.We report here a unique mechanism by which monocytic (M)-MDSCs are spared, allowing them to polariz

192 CD14(pos)HLA-DR(low/neg) monocytic (M)-MDSCs were expanded in intensive care unit

193 and mice: polymorphonuclear (PMN)-MDSCs and monocytic (M)-MDSCs.

194 ved suppressor cells (MDSC) include immature monocytic (M-MDSC) and granulocytic (PMN-MDSC) cells tha

195 TING activation is immunosuppressive due to (monocytic) M-MDSC infiltration, which results in tumor r

196 In addition, 2 populations of monocytic macrophages were observed that differed in ter

197 o differential and reduced expression of the monocytic marker, Ly6C, and granulocytic marker, Ly6G.

198 c(+) CD11b(+) AMs, and these cells expressed monocytic markers Ly6C, CX3CR1, and CD115, suggesting mo

199 D11c(+) CD11b(+) AM subpopulation expressing monocytic markers, a unique inflammatory signature, and

200 Importantly, the presence of monocytic MDS-PA at diagnosis anticipated greater risk o

201 We investigated the clinical significance of monocytic MDS-PA in a larger series of 1252 patients enr

202 t enhances the immunosuppressive function of monocytic MDSC (M-MDSC), although tumor development is d

203 cumulation of polymorphonuclear MDSC but not monocytic MDSC (M-MDSC), and decreased polymorphonuclear

204 mulation of granulocytic MDSC (grMDSCs) over monocytic MDSC (moMDSCs).

205 CD11bCD33CD14CD15HLA-DR (monocytic MDSC [M-MDSC]) and CD11bCD33CD14CD15HLA-DR (mo

206 Two major MDSC subsets, including monocytic MDSC and granulocytic MDSC, have been describe

207 (+)Ly6-G(-)Ly6-C(+) monocytic subtypes, with monocytic MDSC exhibiting higher T cell-suppressive func

208 Moreover, monocytic MDSC have the plasticity to differentiate into

209 , peptibodies depleted both granulocytic and monocytic MDSC subsets.

210 deletion antagonized the differentiation of monocytic-MDSC (M-MDSC) to macrophages and re-routed M-M

211 ate cells (HSC) have been reported to induce monocytic-MDSC from mature CD14(+) monocytes in a contac

212 Frequency of DC-HIL(+) monocytic MDSCs (CD14(+)HLA-DR(no/low)) in blood and ski

213 15(-)MDSCs), >15% early-stage MDSCs and >40% monocytic MDSCs (HLA-DR(-)CD14(+)MDSCs).

214 s from severe liver damage by recruitment of monocytic MDSCs and maintaining a balance between IL-1be

215 ne a functional role of CREMalpha in hepatic monocytic MDSCs for the pathogenesis of immune-mediated

216 Accumulation of CD14(+)HLA-DR(low) monocytic MDSCs has been described in newly diagnosed AM

217 Notably, monocytic MDSCs in Spp1(-/-) mice were less suppressive

218 uiting both CCR4(+) Treg and CCR2(+)Ly-6C(+) monocytic MDSCs in this disease setting.

219 that CCR4-deficient Treg and CCR2-deficient monocytic MDSCs were defective in glioma accumulation.

220 We demonstrated augmentation of monocytic MDSCs whose suppression of not only T-cell, bu

221 G1-expressing cells were mainly immature and monocytic MDSCs, which provides information to better un

222 -cell PD-1 expression and reduced numbers of monocytic MDSCs.

223 nt mice failed to maximally accrue Tregs and monocytic MDSCs.

224 rophages by blocking the association between monocytic membrane-bound TM and CD14.

225 We demonstrate here that monocytic (mMDSC) and granulocytic (gMDSC) subsets of my

226 In human epithelial DLD-1 and monocytic Mono Mac 6 cells resveratrol decreased the exp

227 d PD-1+CD8+; 95% CI, 1.13-8.35; P = .01) and monocytic myeloid derived suppressor cells (mMDSC) (95%

228 L-10-GFP reporter mice, we showed that blood monocytic myeloid-derived suppressive cells mediate the

229 ILC2s, in turn, activate monocytic myeloid-derived suppressor cells (M-MDSCs) via

230 ved an infiltration of neutrophils, T cells, monocytic myeloid-derived suppressor cells (M-MDSCs), an

231 Interestingly, a subset of monocytic myeloid-derived suppressor cells (MDSCs) also

232 Recruitment of monocytic myeloid-derived suppressor cells (MDSCs) and d

233 C)-treated WT, but not IFNAR-deficient mice, monocytic myeloid-derived suppressor cells (MDSCs) were

234 Monocytic myeloid-derived suppressor cells (mMDSC) are a

235 tinib abrogates cytokine-driven expansion of monocytic myeloid-derived suppressor cells (mMDSC) from

236 Cao et al. report increased numbers of monocytic myeloid-derived suppressor cells (Mo-MDSC) in

237 Recently, CD14(+) HLA-DR(-/low) monocytic myeloid-derived suppressor cells (Mo-MDSCs) ha

238 Human monocytic myeloid-derived suppressor cells (MO-MDSCs) wi

239 ure of the TME by decreasing the presence of monocytic myeloid-derived suppressor cells and increasin

240 2, which resulted in the recruitment of both monocytic myeloid-derived suppressor cells and macrophag

241 r progression by inducing differentiation of monocytic myeloid-derived suppressor cells into highly i

242 ased ERK and P38 MAPK signaling responses in monocytic myeloid-derived suppressor cells, which was pa

243 , including macrophages and granulocytic and monocytic myeloid-derived suppressor cells.

244 of CD33 suggested that these cells belong to monocytic myeloid-derived suppressor cells.

245 cells that produce lymphoid and granulocytic-monocytic (myeloid) lineages is unclear.

246 These results implicate a monocytic origin of CD11c(+) cells in inflamed islets an

247 read, the most prominent among them being of monocytic origin such as tumor-associated macrophages (T

248 a subpopulation of human suppressor cells of monocytic origin, referred to as human monocyte-derived

249 tinal RPE and lipid-filled cells of probable monocytic origin.

250 markers Ly6C, CX3CR1, and CD115, suggesting monocytic origin.

251 n MDMs differentiated in the presence of non-monocytic peripheral blood mononuclear cells due in part

252 mor growth through a mechanism that required monocytic phagocytes and a viral chemokine that recruite

253 Depletion of monocytic phagocytes with clodronate completely prevente

254 Toll-like receptor (TLR)-hyper-inflammatory monocytic phenotype has been implicated as a mechanism o

255 al fluid (CSF) analysis revealed lymphocytic/monocytic pleocytosis, elevated protein concentration, a

256 on peripheral blood T cells and a decreasing monocytic population was observed more frequently in the

257 and T-bet expression in T-cell, NK-cell, and monocytic populations as distinguishing features between

258 New studies suggest that circulating monocytic populations may play a role in mediating the i

259 of myeloid lineages and reduced granulocytic/monocytic populations.

260 ved F4/80(+) Mvarphi population, but not non-monocytic precursor-derived CD103(+) dendritic cells.

261 that suggest that they develop by fusion of monocytic precursors derived from haematopoietic stem ce

262 t differentiation of TAMs in tumor site from monocytic precursors was controlled by downregulation of

263 From human monocytic precursors, we differentiated MGCs that expres

264 liferation, and maturation of their Ly6C(hi) monocytic precursors.

265 e, we show that Cebpa-deficient granulocytic-monocytic progenitors were equally resistant to transfor

266 red bone marrow-derived myeloid cells and in monocytic RAW264.7 cells, the LPS-induced expression of

267 matory phenotype, manifested by an increased monocytic release of cytokines after an inflammatory ins

268 s and provide a novel strategy to reactivate monocytic reservoirs with BETi during cART.IMPORTANCE Br

269 This analysis confirmed increased monocytic Siglec-1 expression in active systemic lupus e

270 ovide an overview of the mechanisms by which monocytic subpopulations contribute to angiogenesis in t

271 granulocytic cell populations of MDSCs, the monocytic subset was the predominant source of OPN.

272 +) granulocytic and CD11b(+)Ly6-G(-)Ly6-C(+) monocytic subtypes, with monocytic MDSC exhibiting highe

273 ulation of cell death pathways, we found the monocytic suppressor-cell subset, but not the granulocyt

274 Monocytic suppressors mediate T cell suppression, wherea

275 Monocytic suppressors tolerate the absence of MCL-1 prov

276 e unequivocal identification of ABA within a monocytic T helper 1 (THP-1) cell line, using lumogallio

277 ablation of miRs 135b, 190, and 422a in the monocytic THP-1 cell line.

278 molecule 1 expression, resulting in reduced monocytic THP-1 cell recruitment in vitro.

279 d BT-549) inhibited the recruitment of human monocytic THP-1 cells and primary human macrophages.

280 experiments or RNA knockdown indicated that monocytic THP-1 cells and primary human neutrophils requ

281 teract with the cyclin A-CDK1-CDK2 complexin monocytic THP-1 cells and primary monocyte-derived macro

282 article, we report that retreatment of human monocytic THP-1 cells and primary monocytes with pathoge

283 n recruited a significantly higher number of monocytic THP-1 cells compared with old skin ex vivo.

284 Human monocytic THP-1 cells stimulated with MRP8/MRP14 express

285 When we treated monocytic THP-1 cells with ethionine, their transcriptio

286 Unlike monocytic THP-1 cells with prominent nuclear localizatio

287 urine bone marrow-derived macrophages, human monocytic THP-1 cells, phorbol 12-myristate 13-acetate-d

288 In monocytic THP-1 cells, the R143A virus, but not the wild

289 acts prepared from in vitro propagated human monocytic THP-1 cells, which were used as a model cell l

290 the production of various cytokines in human monocytic THP-1 cells.

291 FRbeta(+) macrophages and FRbeta-transduced monocytic THP-1 cells.

292 In human monocytic (THP-1) cells, ASHW was found to be biocompati

293 Conversely, overexpression of VentX in monocytic THP1 cells accelerated their differentiation t

294 40%, respectively (p < 0.05), and attenuated monocytic tissue factor expression by 33% (p < 0.001).

295 Monocytic TLR-induced cytokine patterns were shared amon

296 man donors, but it is drastically reduced in monocytic tumor cells, THP-1, and U937, rendering them i

297 We generated monocytic U937 cell lines stably expressing WT SAMHD1 or

298 and nonsmoking control subjects, or of human monocytic U937 cells exposed to cigarette smoke extract

299 human primary macrophages and differentiated monocytic U937 cells, in which occludin silencing result

300 pithelial MKN45 and AZ-521 but also in human monocytic U937 cells.