ライフサイエンスコーパス: monocyte

1 ss chemokine and integrin receptor levels on monocytes.

2 arge changes in the transcriptional state of monocytes.

3 MV drugs that prevent the spread of infected monocytes.

4 ting increased transendothelial migration of monocytes.

5 being the primary PI3K isoform found within monocytes.

6 antly on human natural killer (NK) cells and monocytes.

7 nfections and abnormal expression of CD56 by monocytes.

8 ytes in the bloodstream, namely the slan(+) -monocytes.

9 y, to reshape canonical Akt signaling within monocytes.

10 ity and accelerated apoptosis of infiltrated monocytes.

11 MV rapidly induced autophagy within infected monocytes.

12 rophils and the infiltration of inflammatory monocytes.

13 ed phenotypical and functional transition of monocytes.

14 anscriptional variability between individual monocytes.

15 ) pathway, expressing SIRPA, formed DC3s and monocytes.

16 htly clearance of fibrillar alphaSN by human monocytes.

17 filtration of ACE10 as compared to wild-type monocytes (~3-fold increase; P < 0.05) led to reductions

18 may be produced by a subset of inflammatory monocytes(5,6), lymphopenia(7,8) and T cell exhaustion(9

19 eases were also apparent for lymphocytes and monocytes, accompanied by locally elevated plasma levels

20 We measured monocyte activation and gene expression, monocyte-derive

21 gs therefore identify patterns of T-cell and monocyte activation that occur after BCG vaccination but

22 ation suppressed LPS- or MSU crystal-induced monocyte activation, a process depending on the intracel

23 0.27 s-1; P = .003), and heightened systemic monocyte activation.

24 P on endothelial inflammation and subsequent monocyte adhesion is KLF2 dependent.

25 rial WSS-induced CCL2 production and reduced monocyte adhesion, both in vitro and in human LSV ex viv

26 rrier, compromised angiogenesis and enhanced monocyte adhesion.

27 r vascular smooth muscle cells and decreased monocytes adhesion to endothelium, as well as reducing T

28 t increased platelet activation and platelet-monocyte aggregate formation are observed in severe COVI

29 whereas enhanced CD4+ T cell maturation and monocyte aggregation are features of HAM, reflecting wid

30 ncreased expression levels of alpha7nAChR in monocytes, alveolar and interstitial macrophages.

31 is PGA persisted longer in high m.w. form in monocyte and iDC cultures than the other PGAs.

32 patrolling monocytes but preserve classical monocyte and macrophage numbers and functions.

33 e that dampening gene expression profiles of monocyte and neutrophil activation characterize clinical

34 e infusion, and both catecholamines promoted monocyte and neutrophil phagocytosis.

35 ion of CX3CR1-CCR2 signaling attenuated both monocyte and neutrophil trafficking to the CP and cortex

36 d no detectable alpha7nAChR in granulocytes, monocytes and alveolar macrophages, and low expression l

37 uclear cell infiltration (CD11b(+) Ly-6c(hi) monocytes and CD11b(+) Gr1(+) neutrophils).

38 The authors conclude that circulating monocytes and DCs migrate from the blood into the inflam

39 connexin 43-containing gap junctions between monocytes and DCs.

40 6 + T cells, CD56(dim) natural killer cells, monocytes and dendritic cells were not reduced in number

41 by other 'professional' phagocytes (such as monocytes and dendritic cells) and 'non-professional' ph

42 lucidate the underlying heterogeneity within monocytes and dissect how Lyn deficiency affects monocyt

43 okine receptor type 2 (CCR2) is expressed on monocytes and facilitates their recruitment to tumors.

44 hould quantify TME components, in particular monocytes and granulocytes, which are often ignored in m

45 is subsp. chungkookjang and B. licheniformis Monocytes and immature dendritic cells (iDCs) responded

46 d an interferon-stimulated gene signature in monocytes and increased HLA-DR, CD80, CD86, and PD-L1 ex

47 CaSR expression in these monocytes and local [Ca(2+)] in afflicted joints are inc

48 t inherent differences in Ly6c(Hi) classical monocytes and Ly6c(Lo) non-classical monocytes determine

49 Importantly, we found that peripheral monocytes and lymphocytes do not express substantial amo

50 Peripheral immune cells, such as monocytes and lymphocytes, have also been found to play

51 bited elevated levels of circulating Ly6C(+) monocytes and macrophage-derived inflammatory cytokines.

52 demonstrated specific expression of CCR2 on monocytes and macrophages.

53 We show that a higher frequency of monocytes and monocyte-derived cells presented the MHC c

54 Human monocytes and mouse macrophages in tumor cocultures exhi

55 tes exhibited proinflammatory features, both monocytes and neutrophils showed transcriptional evidenc

56 ed a sustained myeloid infiltrate (including monocytes and neutrophils) with increased RNA expression

57 inflammatory cytokine response by recruited monocytes and other cells that controls infection.

58 ded into 2 major subsets termed conventional monocytes and patrolling monocytes (pMo) but recent syst

59 e, and expression of inflammatory markers in monocytes and plasma.

60 pathway activation patterns in conventional monocytes and pMos revealed distinct baseline signaling

61 nature; recruitment of low HLA-DR expressing monocytes and regulatory T-cells; and transcription of i

62 Monocytes and T cells from blood and livers of PSC patie

63 This study demonstrates that circulating monocytes and T cells of patients with HF harboring clon

64 The complex formation of monocytes and T cells was also elevated in OSAS patients

65 in order to ensure the survival of infected monocytes and thus facilitate viral dissemination within

66 Circulating platelet-neutrophil, -monocyte, and -T-cell aggregates were all significantly

67 cytokine/chemokine footprint from the naive monocyte, and that TNF-alpha was the most sensitive cyto

68 epithelial cells, NKT, MAIT, TCR-gammadelta, Monocytes, and CD8 + T-cells that are related to both ge

69 ed infiltration of neutrophils, inflammatory monocytes, and T cells, and increased activation of STAT

70 tors are highly expressed on neutrophils and monocytes, and their activation promotes the migration o

71 The enhanced monocyte apoptosis in CMH-treated mice was paralleled by

72 Monocytes are a heterogeneous population of three distin

73 Ag+ monocytes are an essential source of IL-12 for both inna

74 In atherosclerosis, macrophages and monocytes are exposed to inflammatory cytokines, oxidize

75 Monocytes are innate immune cells essential for host pro

76 Our data suggests that newborn monocytes are intrinsically impaired in extravasation th

77 ated macrophages (TAMs) recruited from blood monocytes are key in establishing an immunosuppressive t

78 is the induction of monocyte survival, where monocytes are normally short-lived cells.

79 Monocytes are rapidly recruited to sites of diabetic com

80 n reprogramming in bone marrow-derived (BMD) monocytes as early as 4 days of recovery from EHS and as

81 ssociated with higher frequencies of M2-like monocytes, as determined by expression of CD206 and CD16

82 Transcriptome analysis of circulating monocytes at baseline showed various differentially expr

83 g IL-6, CXCL10, CXCL11, IFNgamma, IL-10, and monocyte-attracting CCL2, CCL7 and CCL8, was particularl

84 ng CD4 + effector memory T cells, as well as monocytes, B cells and stromal fibroblasts.

85 s defective in chemotaxis of neutrophils and monocytes both in vitro and in vivo.

86 Systemic EP2 antagonism prevented monocyte brain infiltration and provided broader rescue

87 E2 (-/-) mice lack nonclassical patrolling monocytes but preserve classical monocyte and macrophage

88 ered surface expression of integrin CD11b on monocytes by 20+/-5% (all P<5.0x10(-2)).

89 n of chemokines that attract neutrophils and monocytes by 60% to 80% and lowered surface expression o

90 nflammatory cytokine production in recruited monocytes by enhancing Toll-like receptor (TLR)-induced

91 with impaired recruitment of macrophages and monocytes (Ccr2-/- mice), the absence of CD68+ cells (ma

92 A global knockout of the receptor for monocyte chemoattractant protein (CCR2) prevented excess

93 sion of proinflammatory cytokines (including monocyte chemoattractant protein 1, tumor necrosis facto

94 reduced astrogliosis, interleukin-1beta, and monocyte chemoattractant protein-1, suggesting a paracri

95 ed pulp fibroblasts transiently produced the monocyte chemoattractants CCL2 and CCL7, thereby contrib

96 except that tumor necrosis factor alpha and monocyte chemotactic protein 1 expression was only eleva

97 genase 1 hypoxia-inducible factor 1 (HIF-1), monocyte chemotactic protein 1, transforming growth fact

98 g/mL vs 245.4 pg/mL; P = .012) and decreased monocyte chemotactic protein-1 (MCP-1) (513.3 pg/mL vs 8

99 this study, we report that immune regulator Monocyte chemotactic protein-1-induced protein 1 (MCPIP1

100 nt signal transduction pathways that control monocyte chemotaxis can unravel potential targets for pr

101 MCP-1-induced monocyte chemotaxis is a crucial event in inflammation a

102 ne if the sensing of hypoxia by nonclassical monocytes contributes to the development of PH, mice lac

103 re, an RA-responsive gene signature in human monocytes correlates with an immunosuppressive TME in mu

104 as were low albumin level, lymphocyte count, monocyte count, and ratio of peripheral blood oxygen sat

105 Both CD16- and CD16+ newborn monocytes demonstrated lower adherence and extravasation

106 Newborn monocytes demonstrated significantly lower surface expre

107 f C-miR146a oligonucleotide alleviated human monocyte-dependent release of IL-1 and IL-6 in a xenotra

108 in the liver, with a small proportion of C3 monocyte derived and kidney derived, he proceeded to sim

109 long a CCL2/CCR2 axis and differentiate into monocyte-derived alveolar macrophages (Mo-AMs), which is

110 g, there is emerging evidence for a role for monocyte-derived APC (MoAPC) in tissue-resident memory T

111 r inflammatory conditions, when additionally monocyte-derived cells (MCs) become competent antigen-pr

112 how that a higher frequency of monocytes and monocyte-derived cells presented the MHC class I-restric

113 erm potentiation and long-term repression of monocyte-derived cytokine responses, and short-term as w

114 Aspergillus-infected monocyte-derived DCs and neutrophils recruit pDCs, which

115 gs show that B. miyamotoi is phagocytosed by monocyte-derived DCs, causing upregulation of activation

116 e in a mouse food allergy model and on human monocyte-derived dendritic cells (moDCs) and PBMCs.

117 red monocyte activation and gene expression, monocyte-derived exosome micro-ribonucleic acid (miRNA)

118 g the roles of tissue-resident and recruited monocyte-derived macrophage subsets.

119 xpression of 5'-tRNA half molecules in human monocyte-derived macrophages (HMDMs).

120 -HT(7) expression restricted to M-CSF-primed monocyte-derived macrophages (M-MO).

121 ssion in human alveolar macrophages (AM) and monocyte-derived macrophages (MoDM).

122 ) and proinflammatory (GM-CSF-treated) human monocyte-derived macrophages and microglia using RNA seq

123 e expression of SPIC transcription factor in monocyte-derived macrophages and promotes their differen

124 ell loss was compensated by gain of adjacent monocyte-derived macrophages that exhibited convergent e

125 on and subsequent territorial restriction of monocyte-derived macrophages to infarct tissue.

126 derived from human intestinal organoids with monocyte-derived macrophages, in a gut-on-a-chip platfor

127 the signaling and function of primary human monocyte-derived macrophages, using a C5aR2 agonist (Ac-

128 teady-state counterpart of these cells to be monocyte-derived macrophages.

129 lactate increases IL-10 production by human monocyte-derived macrophages.

130 e secretion in THP-1 cells and primary human monocyte-derived macrophages.

131 Accumulation of these nonclassical monocyte-derived pulmonary interstitial macrophages arou

132 nstantly alter lung immunity by contributing monocyte-derived, recruited cells to the AM population.

133 e efficiently than all other macrophages and monocytes despite equivalent infections through enhanced

134 assical monocytes and Ly6c(Lo) non-classical monocytes determine susceptibility to perinatal hepatic

135 Monocyte differentiation under conditions of inflammatio

136 Circulating monocytes displayed an enhanced inflammatory gene expres

137 Intravenously injected monocytes displayed antitumor activity superior to DC va

138 Microbe-stimulated monocytes drive Th17 differentiation in vitro and induce

139 and CCL4 as well as resistin, which augments monocyte-endothelial adhesion.

140 IL-10-regulated genes are involved in monocyte energy homeostasis, migration, and trafficking

141 Here we show that monocytes engulf CPPs via macropinocytosis, and this pro

142 llary bed, we show that the dynamics of THP1 monocytes evolves along successive capillary-like channe

143 Although CF monocytes exhibited proinflammatory features, both monoc

144 Monocyte exosomes from coinfected persons increased in m

145 Consequently, circulating monocytes express fewer IFN-stimulated genes and become

146 tion of infectious agents by neutrophils and monocytes, followed by resolution and repair through tis

147 brain data and granulocytes/T cells/B cells/monocytes for the blood data.

148 e 977 miRNA-sequencing profiles from primary monocytes from individuals of African and European ances

149 Further, we find that monocytes from malaria patients express active caspases-

150 , we identified, in both CD56(+) and CD56(-) monocytes from MDS patients, several abnormalities that

151 m cells (HSCs) and distinguishes HSC-derived monocytes from microglia and other tissue-resident macro

152 om sepsis, and prevent IL-1beta secretion by monocytes from patients with CAPS.

153 Previously, we showed that serum and monocytes from patients with CF exhibit an enhanced NLRP

154 of BTK inhibitors such as ibrutinib and for monocytes from patients with chronic lymphocytic leukemi

155 reduced c-MAF expression in macrophages and monocytes from patients with non-small cell lung cancer

156 crophages (BMDMs) from BTK-deficient mice or monocytes from patients with X-linked agammaglobulinemia

157 Upon stimulation with microbes, monocytes from PSC patients produced significantly more

158 ident alveolar macrophages are depleted, and monocytes from the bone marrow (BM) traffic to the lungs

159 ted in a significant reversal of the altered monocyte function 6 mo after anthelmintic therapy.

160 In steady state, classical monocytes give rise to vasculature-resident cells that p

161 ifferentiation of hematopoietic cells to the monocytes has been well established, the underlying mech

162 Monocytes have traditionally been divided into 2 major s

163 ium and purple for CD163-positive (CD163(+)) monocytes/histiocytes.

164 ich ablate a specific subset of hematogenous monocytes (hMos).

165 Intermediate monocytes (iMo; CD14(+)CD16(+)) increase in number in th

166 2i, which blocks CCR2-mediated chemotaxis of monocytes in a syngeneic mouse T-cell lymphoma in skin.

167 mplifying the hypoxic stress manifest within monocytes in acute inflammatory lesions.

168 limitations and study the role of patrolling monocytes in melanoma metastasis to lungs, we generated

169 accumulation of neutrophils and inflammatory monocytes in miR-155(-/-) mice.

170 these results point to a pathogenic role of monocytes in patients with PSC.

171 we identified IGFBP7, a protein secreted by monocytes in response to parasite stimulation, as a rose

172 en identifies a subset of non-classical (NC) monocytes in the bloodstream, namely the slan(+) -monocy

173 otal to these responses, implicating CD14(+) monocytes in the cholinergic inflammatory reflex.

174 we present such a model and demonstrate that monocytes in the presence of GM-CSF, TGF-beta1, and the

175 cologic inhibition of Ly6c(Lo) non-classical monocytes in this setting restored susceptibility to RRV

176 ike receptor-induced cytokine production and monocyte-induced T-cell proliferation.

177 stroke, we find that Cxcr4 promotes initial monocyte infiltration and subsequent territorial restric

178 in the MM6 cell line and of peripheral blood monocytes, inhibit an apparently constitutive Dicer prot

179 ntly increased together with CD14(+) CD16(+) monocytes, innate lymphoid cells, and natural killer cel

180 g cells (APCs) including dendritic cells and monocytes instruct naive T cells to differentiate into v

181 osure of LSVs to acute arterial WSS promoted monocyte interactions with the vessel lumen.

182 Hepatitis C virus SVR decreased monocyte interferon genes MX1, IFI27, and CD169 in coinf

183 mediating recruitment of Th17 cells and more monocytes into portal tracts.

184 ing axis drives the migration of circulating monocytes into the tumor microenvironment, where they ma

185 development and function of neutrophils and monocytes is primarily governed by the granulocyte colon

186 ivation, polarization, and function of human monocytes isolated from individuals with LTBI with (n =

187 TLR2 expression on CD14 + + classical monocytes isolated in an acute phase from DENV-infected

188 parallel, MI increased circulating Ly6C(hi) monocyte levels and recruitment to tumors and depletion

189 Here, we report that the transcriptomes of monocyte-like THP-1 cells and macrophage-like THP-1 cell

190 to yeast cells' transition inside of a human monocyte-like THP-1 cells line.

191 Furthermore, a rare cell population with monocyte-like transcriptional features was associated (P

192 scriptome analyses suggest that the Ly6C(lo) monocyte lineage regulates PH through complement, phagoc

193 oxia-inducible factor-1alpha in the Ly6C(lo) monocyte lineage were exposed to hypoxia.

194 ells, specifically cells of the nonclassical monocyte lineage, play a direct role in the pathogenesis

195 t the antitumor efficacy of undifferentiated monocytes loaded with protein or peptide Ag.

196 lular subsets: pro-inflammatory or classical monocytes (Ly6c(Hi)) and pro-reparative or non-classical

197 y6c(Hi)) and pro-reparative or non-classical monocytes (Ly6c(Lo)).

198 tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associa

199 the direct effect of IL-33-ST2 signaling on monocyte/macrophage differentiation, self-renewal and re

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

201 nduced decreases in T cells and cells of the monocyte/macrophage lineage.

202 Two cell lines were of monocyte/macrophage origin, and tumors formed in vivo in

203 s, except for significantly higher levels of monocyte/macrophage proteins in SAGN-mainly lysozyme and

204 onuclear phagocyte system (MPS; progenitors, monocytes, macrophages, and classical dendritic cells) a

205 ion within defined isolated cells, including monocytes, macrophages, and DCs isolated from specific t

206 d invariant (MAIT), and NKT cells as well as monocytes, macrophages, and epithelial cells).

207 al component of innate immunity and comprise monocytes, macrophages, dendritic cells, and granulocyte

208 ardiac myocytes and inflammatory cells, like monocyte/macrophages, cellular settings where these epig

209 rthermore, AREG's effects on renal cells and monocytes/macrophages (M/M) were analyzed.

210 Tie2-expressing monocytes/macrophages (TEMs) are a distinct subset of pr

211 neutrophilia only in patients with COPD and monocytes/macrophages and lymphocytes in both patients w

212 ntial increment of noninflammatory Ly-6C(Lo) monocytes/macrophages in the ischemic brain along with t

213 Furthermore, blockage of nSMase in monocytes/macrophages inhibited the secretion of inflamm

214 tivation by pamoic acid reprograms Ly-6C(Lo) monocytes/macrophages to relay a neuroprotective signal

215 ocal inflammation, notably via granulocytes, monocytes/macrophages, and CD1a(int)-expressing cell rec

216 pathogenesis and immunity, including CD14(+) monocytes/macrophages, critical immune response mediator

217 The role of monocytes/macrophages, granulocytes, and interleukin 1 s

218 flammatory T cell differentiation, prolonged monocyte major histocompatibility complex II upregulatio

219 Here we investigate whether monocyte metabolism and function are changed in patients

220 ding conventional dendritic cells (cDCs) and monocyte (MO) subsets, expressed lower levels.

221 Furthermore, monocyte mRNA from EHS mice showed significantly altered

222 signatures of CD4 T, CD8 T, B, and NK cells, monocytes, myeloid dendritic cells (mDCs), and plasmacyt

223 erations in the cytokine milieu, macrophages/monocytes, natural killer cells, T cells, and neutrophil

224 ssociated with type 2 innate lymphoid cells, monocytes, neutrophil trafficking, and T effector cells.

225 al titer and correlates with infiltration of monocytes, neutrophils and activated T cells.

226 identified that circulating lymphocytes and monocytes of individuals simultaneously affected by T2DM

227 Monocytes of infected HG patients and infected non-HG co

228 showed that mitophagy was inhibited in blood monocytes of patients with sepsis as compared with nonse

229 oclonal antibodies to eliminate neutrophils, monocytes, or both.

230 rrelates AM function with their embryonic or monocyte origin.

231 In addition to circulation-derived monocytes, other non-microglial central nervous system (

232 Glomerular endothelium and non-classical monocytes overexpressed a distinct chemokine axis, which

233 recruited NK cells poorly and drove moderate monocyte phagocytic activity, both likely compromised be

234 tor functions, including NK cell activation, monocyte phagocytosis, and complement activity, all of w

235 Monocytes play an important role in the initiation and r

236 Because Ly6C(low) patrolling monocytes (PMo) behave as housekeepers of the vasculatur

237 termed conventional monocytes and patrolling monocytes (pMo) but recent systems immunology approaches

238 thin these cells, and much of what regulates monocyte population homeostasis remains unknown.

239 ge progenitors were derived from granulocyte monocyte precursors (GMPs) and could develop into granul

240 d activation profiles of dendritic cells and monocytes present in the blood and lung of COVID-19 pati

241 nd differentiation skewed toward granulocyte-monocyte progenitors (GMP) during joint and intestinal i

242 eased CD4+ lymphocyte programmed death-1 and monocyte programmed death-ligand-1 expression in most st

243 , after the RMs niche is emptied, peripheral monocytes rapidly differentiate into BMRMs, with the CX3

244 We found that granulocytes and monocytes rapidly replaced macrophages and dendritic cel

245 Monocytes recruited to the glomerular vasculature did no

246 Paired blood exchange tracked the fate of monocytes recruited to the injured kidney.

247 MSU failed to trigger neutrophil and monocyte recruitment in Cd44(-/-) mice and lower IL-1bet

248 and if so how these N-glycans contribute to monocyte recruitment is not known.

249 ously infected with S. aureus, showed faster monocyte recruitment, increased bacterial killing and im

250 kines, or adhesion molecules associated with monocyte recruitment, IRAK-M was necessary for CCR2 upre

251 tions revealed enrichment of neutrophil- and monocyte-related pathways.

252 pha+ monocytes, suggesting that CMH enhances monocyte removal by amplifying the hypoxic stress manife

253 -18 (but not IL-1beta) production from human monocytes requires cooperative Toll-like receptor and IF

254 lls including progenitors, circulating blood monocytes, resident tissue macrophages, and dendritic ce

255 sed PD-1 and PD-L1 expression in T cells and monocytes, respectively, which was linked to the severit

256 uch as whether CCL2 or IL12 define effective monocyte responses to the parasite.

257 gh informative, population-level averages of monocyte responses to Toxoplasma have sometimes produced

258 The impaired monocyte secretome demonstrated a distinct cytokine/chem

259 TEMs) are a distinct subset of proangiogenic monocytes selectively recruited to tumors in breast canc

260 to blocking brain recruitment of blood-borne monocytes.SIGNIFICANCE STATEMENT Unabated seizures reduc

261 We generated mice with macrophage/monocyte-specific deletion of YAP (YAP( KO) ) or Toll-li

262 tic cells towards a weaker immune-responsive monocyte state and that this anergic-like state is cruci

263 experiments revealed that GM-CSF blockage in monocytes stimulated production of the chemokine CXCL-11

264 alyzed the transcriptomes of eight different monocyte subgroups derived from the brain and the blood

265 ctively, which was linked to the severity of monocyte subset alterations.

266 cytes and dissect how Lyn deficiency affects monocyte subset composition, signaling, and gene express

267 Furthermore, the classical monocyte subset of DNMT3A mutation carriers showed incre

268 Mass cytometric analysis of monocyte subsets and signaling pathway activation patter

269 distribution of the CD14/CD16 characterized monocyte subsets in peripheral blood as well as their PD

270 ce may allow for the recruitment of specific monocyte subsets to sites of inflammation, and how furth

271 preferential binding to the proinflammatory monocyte subtype and partially via SR-BI (scavenger rece

272 ralleled by increased numbers of HIF-1alpha+ monocytes, suggesting that CMH enhances monocyte removal

273 ting the mechanisms by which HCMV stimulates monocyte survival is an important step to the developmen

274 n cytomegalovirus (HCMV) is the induction of monocyte survival, where monocytes are normally short-li

275 lecule CD58, all of which may be involved in monocyte-T-cell interactions.

276 ury in a subset of ASD that may benefit from monocyte-targeted treatments.

277 Platelet activation and monocyte TF expression were associated with markers of c

278 g platelet activation and platelet-dependent monocyte TF expression, which were associated with COVID

279 ted white blood cell counts (neutrophils and monocytes), thereby increasing atherosclerosis severity,

280 igh neutrophil to lymphocyte ratio (NLR) and monocyte to lymphocyte ratio (MLR) are respectively asso

281 In vitro, we exposed human primary monocytes to (nor)adrenaline for 24 hours, after which c

282 We sought to comprehensively profile monocytes to elucidate the underlying heterogeneity with

283 f eosinophils, neutrophils, and inflammatory monocytes to lung metastases.

284 etermine the contribution of neutrophils and monocytes to resolution of the condition and the subsequ

285 nity, in which sUA modulates the capacity of monocytes to respond to danger signals.

286 (ii) adoptive transfer of CD115+-ACE10/GFP+ monocytes to the peripheral blood.

287 y across thousands of myeloid enhancers in a monocyte-to-macrophage cell fate model.

288 As such, a molecular understanding of human monocyte-Toxoplasma interactions can expedite the develo

289 hallenge, mice lacking IRAK-M have decreased monocyte trafficking and reduced Mo-AMs in their lungs.

290 These data indicate that IRAK-M regulates monocyte trafficking by increasing the expression of CCR

291 he expression of CCR2, resulting in enhanced monocyte translocation into the lung, Mo-AM differentiat

292 We also find that monocytes undergo M2 polarization in the tumor region an

293 ta regulate plasmacytoid dendritic cells and monocytes via TLR7 and MyD88 signaling to protect from a

294 A core of fibrinogen and monocytes was found in 39 (93%) white-centered hemorrhag

295 urvival of autophagy-inhibited HCMV-infected monocytes was rescued when MLKL and RIPK3 were suppresse

296 Monocytes were isolated from peripheral blood to determi

297 Skap2-/- neutrophils and monocytes were present in infected lungs, and the neutro

298 Pretransplant, M-MDSC, and monocytes were similar in KTRs and healthy volunteers.

299 MDSC [M-MDSC]) and CD11bCD33CD14CD15HLA-DR (monocytes), were defined by flow cytometry.

300 he terminal differentiation path of slan(+) -monocytes, which is relevant for inflammatory diseases a

301 trate that n-apo AI binds to neutrophils and monocytes, with preferential binding to the proinflammat