ライフサイエンスコーパス: myeloid cell

1 3 is predominantly expressed in lymphoid and myeloid cells.

2 NA-mediated inflammasome activation in human myeloid cells.

3 issue-restricted PD-L2 was regulated only in myeloid cells.

4 tant role in the expression of C/EBPalpha in myeloid cells.

5 at the tumor site, transfecting intratumoral myeloid cells.

6 g expression of PD-L1 in bone marrow-derived myeloid cells.

7 ective gene knockout was achieved in various myeloid cells.

8 orders associated with hyperproliferation of myeloid cells.

9 ant with an influx of CCDC88B(+)lymphoid and myeloid cells.

10 e neutrophils and hyperplasia of bone marrow myeloid cells.

11 rs to be a key regulator of HIV infection in myeloid cells.

12 atory molecules, IL-1beta and S100A9, by the myeloid cells.

13 in levels, the essential inducers of iNOS in myeloid cells.

14 multiple signaling pathways of lymphoid and myeloid cells.

15 enhanced by coordinated recruitment of host myeloid cells.

16 vation of the toll-like receptor 4 (TLR4) on myeloid cells.

17 ped with the transcriptional signature of HD myeloid cells.

18 by activating gut and mesenteric lymph node myeloid cells.

19 howing a competitive advantage for BCAP(-/-) myeloid cells.

20 inhibitory hFcgammaR expression on specific myeloid cells.

21 clear factor kappaB (NF-kappaB) in microglia/myeloid cells.

22 ell lineage but enacts commitment toward the myeloid cells.

23 rized by the uncontrolled growth of immature myeloid cells.

24 igger proinflammatory cytokine expression in myeloid cells.

25 nd TNF (tumor necrosis factor) production by myeloid cells.

26 numbers of splenic CD11b(+)Gr-1(+) immature myeloid cells.

27 an important regulator of c-Myc function in myeloid cells.

28 plays an important anti-inflammatory role in myeloid cells.

29 turbations to prothrombotic TF activation on myeloid cells.

30 ransforming different types of lung-resident myeloid cells.

31 ulator of many facets of immune responses by myeloid cells.

32 p of HIV-1 replication in T cells but not in myeloid cells.

33 he type I interferon receptor in a subset of myeloid cells.

34 urface expression of PD-L1 in epithelial and myeloid cells.

35 ls and significantly decreased percentage of myeloid cells.

36 ring viral and bacterial infections in human myeloid cells.

37 s, and shuttles them in the cytosol of human myeloid cells.

38 s effect is mediated via the S1PR1 on LysM+ (myeloid) cells.

39 by TREM-1 (triggering receptor expressed on myeloid cells 1) and lipopolysaccharide.

40 Triggering receptor expressed on myeloid cells-1(TREM-1) is a member of the superimmunogl

41 ce receptor triggering receptor expressed on myeloid cells 2 (Trem2 (-/-)) were protected from LCMV-i

42 Triggering receptor expressed on myeloid cells 2 (TREM2) is a single transmembrane molecu

43 Triggering receptor expressed on myeloid cells 2 (TREM2) is a transmembrane protein expre

44 ncoding the triggering receptor expressed on myeloid cells 2 (TREM2) were recently found to increase

45 n Tg-AD and triggering receptor expressed on myeloid cells 2 (Trem2)(-/-) Tg-AD reveals that the DAM

46 gene TREM2 (triggering receptor expressed on myeloid cells 2) confer greatly elevated risk for develo

47 TREM2 (triggering receptor expressed on myeloid cells 2) induced APOE signaling, and targeting t

48 gene TREM2 (triggering receptor expressed on myeloid cells 2).

49 a receptor, triggering receptor expressed on myeloid cells 2, in the increased risk of late onset AD.

50 The protein triggering receptor expressed on myeloid cells-2 (TREM2) is an immunomodulatory receptor

51 herosclerosis, however it's possible role in myeloid cell accumulation and activation is not understo

52 TREM2 deficiency decreases plaque-associated myeloid cell accumulation by reducing cell proliferation

53 nomodulatory receptor with a central role in myeloid cell activation and survival.

54 llel with depression of serum markers of the myeloid cell activation, such as CCL5, CCL11, and C-X-C

55 id not alter immune effector cell numbers or myeloid cell activation.

56 The healthy counterparts of myeloid cells affected by BRAF mutation had a range of d

57 ype reproduced in mice lacking AMPKalpha2 in myeloid cells (AMPKalpha2(DeltaMC)).

58 IL-1beta is produced by myeloid cells and acts as a critical mediator of host de

59 , which reduces proinflammatory signaling in myeloid cells and B cells.

60 d more efficient interactions between aortic myeloid cells and CD4(+) T cells.

61 c burden, and infiltration by CD11b(+)Gr1(+) myeloid cells and CD4(+)CD25(+)FOXP3(+) Tregs, whereas t

62 s acquire pathogenicity and communicate with myeloid cells and cells of the CNS remain unclear.

63 /ID2 signaling may restrict tumor-associated myeloid cells and could potentially be a therapeutic str

64 ators of nuclear factor kappaB activation in myeloid cells and DCs, was shown to control DC activatio

65 sue integrity due to reduced infiltration of myeloid cells and diminished production of pro-inflammat

66 acrophage phenotype by deleting PPARgamma in myeloid cells and found a 5- to 10-fold decrease in gast

67 FR1-dependent accumulation of CD11b-positive myeloid cells and higher expression of the VEGFR1 ligand

68 for GCV to inhibit inflammation in cultured myeloid cells and in a mouse model of multiple sclerosis

69 ed human colorectal tumors for EGFR-positive myeloid cells and investigated their association with pa

70 tial expression of inhibitory FcgammaRIIB on myeloid cells and its differential binding of IgG subcla

71 try and flow cytometry were used to identify myeloid cells and neuronal loss.

72 Responsiveness to IFNgamma by myeloid cells and other haematopoietic cells, including

73 S100A9 inhibits B lymphopoiesis by acting on myeloid cells and promoting the release of inflammatory

74 that Aid loss in mice leads to expansion of myeloid cells and reduced erythroid progenitors resultin

75 alendronate in PLN reversed these effects on myeloid cells and shifted the profile of multi-cytokine

76 In vivo, myeloid cells and their progenitors are an important sit

77 sed exclusively in granulocytes and immature myeloid cells and transforms the topoisomerase II (TOP2)

78 on of PD-L1 expression in tumor-infiltrating myeloid cells and, therefore, reprogramming of PGE2 meta

79 was deficient in both endothelial cells and myeloid cells) and LysM CreNox2KO mice (in which Nox2 wa

80 specific Keap1 disruption (i.e., in T cells, myeloid cells, and dendritic cells) achieved only partia

81 relatively low levels on normal lymphoid and myeloid cells, and in some tissues of nonhematopoietic o

82 ulation of KDR, suppression of proangiogenic myeloid cells, and prevention of low-grade to high-grade

83 activation in NF-kappaB sensor cells, THP-1 myeloid cells, and primary human B cells as well as in m

84 We added BM fat, CD11b(+) myeloid cells, and recombinant S100A9 to B lymphopoiesis

85 ration and permeability of tumor-stimulatory myeloid cells, and suppressed EC-mediated stimulation of

86 dramatic increase in fat, increased CD11b(+) myeloid cells, and upregulated expression of the inflamm

87 oliferation and function by immunoregulatory myeloid cells are an essential means of preventing self-

88 Myeloid cells are central to atherosclerotic lesion deve

89 Myeloid cells are crucial early effectors in organ ische

90 Furthermore, HD myeloid cells are hyper-reactive compared to control.

91 Myeloid cells are known to play an essential role in med

92 Accordingly, RXR-deficient myeloid cells are more efficient in promoting cancer cel

93 port that bone marrow (BM) Gr-1(lo) immature myeloid cells are responsible for the elevated, patholog

94 e contents of this microenvironment, such as myeloid cells, are a major factor in the overall prognos

95 d the kidney, and they implicate BM immature myeloid cells as a key contributor to glomerular dysfunc

96 KDR expression increased in myeloid cells as myeloid-derived suppressor cells (MDSCs

97 r results identify RXR as a regulator in the myeloid cell-assisted metastatic process and establish l

98 trasts with the concept that accumulation of myeloid cells at ischemic and hypoxic sites results from

99 In the absence of IL-27R myeloid cells become hyperactivated, produce pro-inflamm

100 otensin (AT1) receptors in T lymphocytes and myeloid cells blunts the polarization of these cells tow

101 Tet2 expression is increased in intratumoral myeloid cells both in mouse models of melanoma and in me

102 ing IL-4Ralpha and IL-13Ralpha1 give rise to myeloid cells but not T cells.

103 sulfide isomerase (PDI) and TF expression by myeloid cells, but did not require neutrophil extracellu

104 Deletion of EGFR from myeloid cells, but not intestinal epithelial cells, prot

105 s study, we find that activation of NLRP3 in myeloid cells, but not mesenchymal cells triggers chroni

106 progenitor populations produce lymphoid and myeloid cells, but they remain incompletely characterize

107 hlight the neuroprotective nature of certain myeloid cells by emphasizing their therapeutic potential

108 ional deletion of the Tnfaip3 gene in either myeloid cells (by using the lysozyme M [LysM] promotor)

109 immunosuppressive phenotype of infiltrating myeloid cells, by modulating inflammatory gene expressio

110 Bone marrow-derived myeloid cells can accumulate within tumors and foster ca

111 e for the protumoral effects of infiltrating myeloid cells can be used to target established liver me

112 In human CD14(+) myeloid cells, CCDC88B is regulated by cis-acting varian

113 umor gene expression signatures specific for myeloid cell chemotaxis and homeostasis reappeared in BR

114 luate how EGFR expression in tumor cells and myeloid cells contributes to development of colitis-asso

115 rotection allows for the identification of a myeloid cell contribution to tissue repair.

116 enewal ability and leukemogenesis of MLL-Af4 myeloid cells could contribute to the strong B-cell ALL

117 Colony-forming unit numbers, host myeloid cell counts, cell recruitment, cytokine producti

118 ion of multi-lineage capacity in single HSPC myeloid cell cultures, further suggesting a link between

119 n of NFI-A in myeloid progenitors from NFI-A myeloid cell-deficient mice impeded myeloid cell maturat

120 noclonal antibodies, KWAR23 greatly augments myeloid cell-dependent killing of a collection of hemato

121 hin blood and brain tissue was attenuated by myeloid cell depletion after TBI.

122 Systemic myeloid cell depletion with anti-Gr-1 antibody blocked t

123 Mice with deletion of EGFR from myeloid cells developed more severe colitis after DSS ad

124 es PU.1, a transcription factor critical for myeloid cell development and function.

125 molecular transcriptome switch that controls myeloid cell differentiation and maturation and that mal

126 The roles of these receptors in myeloid cells during B cell autoimmune activation remain

127 is is necessary for the generation of mature myeloid cells during homeostatic turnover and immunologi

128 ry to previous reports, that HIF pathways in myeloid cells during inflammation and hypoxia are dispen

129 te-macrophage colony-stimulating factor with myeloid cell dysplasia and ineffective hematopoiesis.

130 er and identify SiglecF(high) neutrophils as myeloid cell effectors of the osteoblast-driven protumor

131 tudy, we demonstrate that deletion of RXR in myeloid cells enhances lung metastasis formation while n

132 nodeficiency virus of macaques) infection of myeloid cells, even in the presence of Vpx.

133 ous population of immunosuppressive immature myeloid cells, expanded during chronic Staphylococcus au

134 iR-155 collaborates with FLT3-ITD to promote myeloid cell expansion in vivo and that this involves a

135 ce lacking IRF3 also developed lung disease, myeloid cell expansion, and T cell cytopenia.

136 evealed that the STING N153S mutation caused myeloid cell expansion, T cell cytopenia, and dysregulat

137 LDL receptor-deficient (Ldlr-/-) mice whose myeloid cells expressed a cleavage-resistant variant of

138 Both peripheral and intestinal myeloid cells expressed INAVA.

139 transient increase in a population of CD11b+ myeloid cells expressing HLA-DR, CD11c, and CX3CR1.

140 ssis Secreted as soluble protein, it targets myeloid cells expressing the CD11b/CD18 integrin and on

141 ls in the stroma of human colorectal tumors; myeloid cell expression of EGFR associated with tumor me

142 Myeloid cell expression of EGFR increases activation of

143 data to foster our understanding of lymphoid/myeloid cell-fate decisions.

144 understood interaction among megakaryocytes, myeloid cells, fibroblasts, and endothelial cells.

145 phoid cells, which then recruit and activate myeloid cells for enhanced killing of mAb-opsonized tumo

146 investigated the precise role of TNFAIP3 in myeloid cells for the development of TH2- and TH17-cell

147 Mice with deletion of EGFR from myeloid cells formed significantly fewer and smaller tum

148 ntiation factor (Endoglin) were increased in myeloid cells from p65 KO tumor, which demonstrated an i

149 Increased expression of EGFR in myeloid cells from the colorectal tumor stroma associate

150 nd 2 (CCL2) into the bloodstream to mobilize myeloid cells from the host bone marrow to the pleural s

151 ay have a "dual effect" on both neuronal and myeloid cell function that could explain a shared propen

152 oid specific HIFs are crucial for aspects of myeloid cell function, including their ability to migrat

153 ation of HIF pathways via deletion of Vhl in myeloid cells had no impact on myeloid trafficking into

154 eNox2KO mice (in which Nox2 was deficient in myeloid cells) had significantly lower BP than littermat

155 3% of non-ALL B lymphocytes, T cells, and/or myeloid cells harbored the BCR-ABL1 fusion in patients w

156 As part of the innate immune system, myeloid cells have diverse roles in blood pressure regul

157 yed by infiltrating monocytes in maintaining myeloid cell homeostasis in the retina following AMD-rel

158 In both B cells and myeloid cells, IL-10 can be produced in response to Toll

159 uld facilitate productive HIV-1 infection in myeloid cells in cis and CD4(+) T cells in trans and thu

160 e for keratinocytes and their interplay with myeloid cells in dengue.

161 The central role of myeloid cells in driving autoimmune diseases and cancer

162 n and functions of infiltrating and resident myeloid cells in GBM, establishing a rationale to target

163 ests a possible role of somatic mutations in myeloid cells in neurodegeneration.

164 ressive inflammation in tumors by recruiting myeloid cells in part via the CCR2 pathway.

165 arity and a restored balance of lymphoid and myeloid cells in peripheral blood.

166 IFITM3 inhibited IL-6 production by myeloid cells in response to replicating and nonreplicat

167 is characterized by accumulation of immature myeloid cells in the bone marrow and phenotypic cellular

168 EGFR-deficient myeloid cells in the colon of DSS-treated LysM-Cre; Egfr

169 ranscription was induced in both T cells and myeloid cells in the heart.

170 We detected EGFR in myeloid cells in the stroma of human colorectal tumors;

171 cer immunity by manipulating the function of myeloid cells in the tumor microenvironment.

172 jugated to Pseudomonas exotoxin A to deplete myeloid cells in vitro and in vivo.

173 e CD11b(+)Gr1(-) and immature CD11b(+)Gr1(+) myeloid cells in vivo Strikingly, although IRF8 was sile

174 suggesting productive infection of CD169(+) myeloid cells in vivo While cell-free HIV-1 infection of

175 tion between endothelial and local CD200R(+) myeloid cells, including activated microglia and infiltr

176 tor (RXR) regulates several key functions in myeloid cells, including inflammatory responses, phagocy

177 -regulation of fatty acid oxidation (FAO) in myeloid cells, including macrophages and granulocytic an

178 background, we showed that Bmal1 deletion in myeloid cells increased the size of atherosclerotic lesi

179 icroenvironment but altered the phenotype of myeloid cells, increased NK cell and Th1 cytokine levels

180 by accumulation of CD11b(+)Gr-1(+) immature myeloid cells, indicating a potential antitumorigenic ef

181 that KRAS(G12D) expression in lung-resident myeloid cells induces pulmonary LCH-like neoplasms compo

182 nd Th1 cytokine levels, and reduced immature myeloid cell infiltrate and blood chemokine levels.

183 Results Myeloid cells infiltrated into the injured cord at 6 and

184 matory milieu with a reduction of pathogenic myeloid cell infiltration and a marked accumulation of e

185 Their ingestion induced modest intestinal myeloid cell infiltration and activation, and release of

186 red as a result of reduced demyelination and myeloid cell infiltration into the CNS tissue.

187 nse as assessed by changes in ear thickness, myeloid cell infiltration, and cytokine and chemokine se

188 ificantly reduced urine abnormalities, renal myeloid cell influx, and NCGN.

189 on of canonical NF-kappaB signaling (p65) in myeloid cells inhibited syngeneic glioblastoma (GBM) thr

190 In addition, TREM2 deficiency reduces myeloid cell internalization of amyloid throughout patho

191 ically, the elevated trafficking of infected myeloid cells into the brain in Ccr7-deficient mice resu

192 PET-MRI allows monitoring of myeloid cell invasion and metabolism.

193 Human cytomegalovirus (HCMV) infection of myeloid cells is closely linked with the differentiation

194 xpression of integrin-linked kinase (ILK) in myeloid cells is critical for the epithelial inflammator

195 show that translation of VEGFA mRNA in human myeloid cells is dictated by a bi-directional interactio

196 The plasticity of myeloid cells is illustrated by a diversity of functions

197 ns, the branching and patrolling activity of myeloid cells is increased, and their phagocytic activit

198 ere, we sought to determine whether c-Myc in myeloid cells is regulated by PRMT1-dependent arginine m

199 Our studies show that TGF-beta signaling in myeloid cells is required for maintenance of vascular he

200 hat amplified ROS production specifically by myeloid cells is sufficient to promote intestinal mutage

201 ne viral gene expressed by latently infected myeloid cells is US28.

202 Myeloid cells, key players in atherosclerosis, take up a

203 with expression of the BCL-2 family members myeloid cell leukemia 1 (MCL-1) and BCL-XL in lymphoma c

204 Myeloid cell leukemia 1 (MCL-1) is a prosurvival BCL-2 p

205 cally associated with elevated expression of myeloid cell leukemia 1 (Mcl1) but not other antiapoptot

206 ed extracellular signal-regulated kinase and myeloid cell leukemia 1 levels.

207 cellular signal-regulated kinase+/BCL-XL(+) /myeloid cell leukemia 1+ signature, deregulated in Alb-R

208 Here, we showed that myeloid cell leukemia sequence 1 (Mcl-1) acts as a funct

209 Committed Hdc(+) myeloid cells lie in close anatomical proximity to MB-HS

210 -PTP1B(-/-) mice lacking PTP1B in the innate myeloid cell lineage displayed a dysregulation of bone m

211 erized by excess accumulation of one or more myeloid cell lineages and a tendency to transform to acu

212 Mice lacking Bim in myeloid cells (LysM(Cre)Bim(fl/fl)) develop a systemic l

213 /f) and Villin-CreER(T2); Egfr(f/f) mice) or myeloid cells (LysM-Cre; Egfr(f/f) mice) on a mixed back

214 phils declined by day 7, while the number of myeloid cells, macrophages, and monocytes did not.

215 om NFI-A myeloid cell-deficient mice impeded myeloid cell maturation and promoted immune repressor fu

216 studies suggest that modulation of Roquin in myeloid cells may reduce both inflammation and bacterial

217 oth together, had no impact on the number of myeloid cells migrating into the eye.

218 TGF-beta, VEGF and SDF-1 abolished VEGFR1(+) myeloid cell migration and fibroblast activation induced

219 uced by CYP4A inhibition decreased VEGFR1(+) myeloid cell migration and fibronectin expression, accom

220 demonstrate the dispensable role of HIFs in myeloid cell migration into the inflamed eye.

221 sensing as a key requirement for long-range myeloid cell migration to intermediate chemokines and pr

222 ing the human resolvin E1 receptor (ERV1) in myeloid cells, monocyte phenotypic shifts to increased p

223 d mice have a population of highly activated myeloid cells not present in laboratory mice.

224 herto unrecognized modulation of basal BP by myeloid cell Nox2, whereas endothelial cell Nox2 regulat

225 ) progenitors proliferated and produced more myeloid cells of both neutrophil and monocyte/macrophage

226 findings indicate that expression of EGFR by myeloid cells of the colorectal tumor stroma, rather tha

227 SMA, implying a differential role of SMN in myeloid cell ontogeny.

228 mutated in ALS/FTD, has an important role in myeloid cells opened the possibility that altered microg

229 stroy tumors by recruiting effectors such as myeloid cells, or targeting immunomodulatory receptors t

230 Myeloid cells play a key role in tumor progression and m

231 n ischemic skeletal muscle, and whether host myeloid cells play a role.

232 the release of ATP, a chemotactic signal for myeloid cells, polyploidization can trigger endoplasmic

233 Instead, perivascular macrophage-like myeloid cells populate the Nrros(-/-) CNS.

234 the inner retina that replenishes the local myeloid cell population in a CCR2-regulated manner.

235 edundantly or by targeting non-T cell or non-myeloid cell populations.

236 Myeloid cells produced more inflammatory cytokines and u

237 EGFR signaling in myeloid cells promoted activation of STAT3 and expressio

238 rowth factor receptor 1 positive (VEGFR1(+)) myeloid cell recruitment and pro-metastatic protein expr

239 il survival, which in turn determine further myeloid cell recruitment and repair potential.

240 ng controls endothelial cells activation and myeloid cell recruitment at early and advanced stages of

241 ncreasing transcription of genes involved in myeloid cell recruitment more than either liver sinusoid

242 cell adhesion molecule 1) genes involved in myeloid cell recruitment was reduced in a majority of TR

243 is revealed greater thrombus weight, length, myeloid cell recruitment, and more neutrophil extracellu

244 ce of GMP and MDP differentiation shapes the myeloid cell repertoire during homeostasis and following

245 ydroxycholesterol (27HC) that acts on immune myeloid cells residing at the distal metastatic sites, t

246 We found that myeloid cell responses to RPE injury occur in stages: (1

247 utput to regulate tissue resolution tone and myeloid cell responses.

248 varian adenocarcinoma, Gadd45b inhibition in myeloid cells restored activation of proinflammatory tum

249 inflammatory monocytes, but not DCs or other myeloid cells, resulted in lower levels of IL-18 and a c

250 A novel role for myeloid cell-specific neuropilin 1 in mitigating sepsis.

251 ivation were monitored in wild-type (WT) and myeloid cell-specific Nrp1 knockout (Nrp1(myel-KO)) mice

252 Here, we reported that myeloid cell-specific Nrp1-deficient mice exhibited enha

253 To address this problem, we generated myeloid cell-specific Nrp1-knockout (Nrp1(myel-KO)) mice

254 , we present evidence that EGFR signaling in myeloid cells, specifically macrophages, is critical for

255 n receptor (KDR), also known as VEGFR2, in a myeloid cell sublineage is necessary for malignant progr

256 ent antitumor activity by targeting multiple myeloid cell subsets that frequently infiltrate tumors.

257 e responses and differential infiltration of myeloid cell subsets.

258 ful tissue repair requires the activities of myeloid cells such as monocytes and macrophages that gui

259 del in which FlnA is selectively depleted in myeloid cells, such as neutrophils, we show that FlnA ne

260 Ablation of Tet2 in myeloid cells suppressed melanoma growth in vivo and shi

261 Loss of acid ceramidase in myeloid cells suppresses intestinal neutrophil recruitme

262 review details the complex interplay between myeloid cells, T cells, and salt in the pathogenesis of

263 ecific deletion of IFN-gammaR2 expression on myeloid cells, T cells, or neurons were completely susce

264 report that mice with deletion of Tgfbr2 in myeloid cells (Tgfbr2(Myeko)) developed cerebrovascular

265 nthase (iNOS) generates nitric oxide (NO) in myeloid cells that acts as a defense mechanism to suppre

266 ration is facilitated by bone-marrow-derived myeloid cells that are recruited to the lung through a C

267 belong to a lineage of adult tissue-resident myeloid cells that develop during organogenesis from yol

268 cted keratinocytes attracts virus-permissive myeloid cells that inadvertently spread DENV infection.

269 Here, we review the subsets of myeloid cells that inhabit the parenchyma, meninges, and

270 Microglia are brain-resident myeloid cells that mediate key functions to support the

271 , as well as the establishment of latency in myeloid cells that results in lifelong infection.

272 cells orchestrate inflammatory responses in myeloid cells through a CD40-ATP-P2X7 pathway.

273 equence to activate C/EBPalpha expression in myeloid cells through a mechanism that is distinct from

274 we identified changes in tumor-infiltrating myeloid cell (TIM) subsets that likely compromise anti-t

275 inflammation and hypoxia are dispensable for myeloid cell tissue trafficking.

276 oblast-derived GM-CSF alerts its neighboring myeloid cells to attract neutrophils and monocytes.

277 ent reduction in the cytokine response of HD myeloid cells to LPS, suggesting that wild-type HTT has

278 phocytes and CXCR1(+), CXCR2(+), and CCR2(+) myeloid cells toward EB-derived blister fluids.

279 -dox treatment also repolarized intratumoral myeloid cells towards an antitumor phenotype.

280 ed an increase in chemotaxis, migration, and myeloid cell trafficking in patients with severe asthma,

281 a-dependent neuroinflammatory events promote myeloid cell trafficking to the brain that reinforces st

282 discovered triggering receptor expressed on myeloid cells (TREM)-2 has been shown to be expressed on

283 ng nucleophosmin-1 (NPM1) mutation generated myeloid cells unfit for normal hematopoiesis but prone t

284 including satellite cells, and infiltrating myeloid cells upon tissue damage.

285 Increasing demand for myeloid cells via lipopolysaccharide (LPS) treatment spe

286 mming infiltrating MCs into antiinflammatory myeloid cells via secretion of TGF-beta2.

287 on of HIV-1 was rescued in IFN-alpha-treated myeloid cells via upregulation of CD169 and a subsequent

288 Surface marker expression of CD11b+ myeloid cells was also assessed.

289 A marked increase of Gr-1(lo) myeloid cells was commonly found in the BM of proteinuri

290 e pattern of involvement of peripheral blood myeloid cells was indistinguishable between LCH and ECD,

291 ulation of CCR5 expression on CD11b(+)Gr1(+) myeloid cells was induced in vitro by CCR5 ligands and o

292 ptic mice with conditionally deficient NFI-A myeloid cells were able to respond to challenge with bac

293 Myeloid cells were characterized in flow cytometric, his

294 Primary ex vivo myeloid cells were isolated from heterozygous patients a

295 Importantly, these myeloid cells were mostly Ly6C(low) monocytes and not Ly

296 of the gene encoding PD-L1 in epithelial and myeloid cells, whereas the gene encoding the more tissue

297 s and production of leukotriene B4 (LTB4) in myeloid cells, which modulate inflammatory arthritis.

298 phopoiesis in vitro by inducing inflammatory myeloid cells, which produce IL-1beta.

299 and thereby enhanced migration of VEGFR1(+) myeloid cells, which were reversed by siRNA or pharmacol

300 ecruitment of T lymphocytes and inflammatory myeloid cells, while peripheral immunity remained intact