ライフサイエンスコーパス: myeloid

1 ue cultures triggered antiviral responses in myeloid and CD4(+) T cells.

2 throid leukemia (AEL) commonly involves both myeloid and erythroid lineage transformation.

3 aggressive growth include interactions with myeloid and fibroblastic cells in the tumour microenviro

4 e severe depression but differed in terms of myeloid and lymphoid cell counts.

5 mune cell homeostasis by shaping the fate of myeloid and lymphoid cells.

6 F1R inhibition by PLX5622 indeed affects the myeloid and lymphoid compartments, causes long-term chan

7 nt leukocytes, which recapitulated the liver myeloid and lymphoid composition, and underwent partial

8 rofile resembling that of tumor infiltrating myeloid and lymphoid populations, but with higher expres

9 We found that myeloid and lymphoid resident immune cells concentrate a

10 et al provide evidence for the existence of myeloid- and lymphoid-dominant human hematopoietic stem

11 including loss of engraftment ability and a myeloid-biased output.

12 characterized by the accumulation of clonal myeloid blast cells unable to differentiate into mature

13 he downregulation of key pathways regulating myeloid cell cycle, maturation and regenerative function

14 capture three distinct biological processes: myeloid cell differentiation, protein phosphorylation an

15 hial epithelial repair, and implicate ST2 in myeloid cell differentiation.

16 ssue and fibroblasts suggests involvement in myeloid cell functions during periodontal inflammation.

17 n lymphoid organ formation, in COPD.Methods: Myeloid cell heterogeneity and phenotype were studied in

18 These results suggest that increased myeloid cell infiltration contributes to autoreactive CD

19 Thus, IRF5 acts as a regulator of myeloid cell inflammatory cytokine production during IAV

20 How myeloid cell lineage affects activation states in respon

21 human TB, and overlap between fibroblast and myeloid cell markers in tissues.

22 T cell engager leads to changes in the host myeloid cell population, both of which contribute to tre

23 To better characterize these different myeloid cell populations, we used long-term in vivo 2-ph

24 ld be targeted in LSCs to normalize leukemic myeloid cell production.

25 ine axis, which may orchestrate inflammatory myeloid cell recruitment and expression of damage mediat

26 oxinemia, thus suggesting that NETs regulate myeloid cell recruitment.

27 ic approaches aimed at resolving detrimental myeloid cell responses in tissues, including those occur

28 Little is known about the roles of myeloid cell subsets in kidney injury and in the limited

29 Increased cellular ATP underpins increased myeloid cell superoxide production and phagocytosis asso

30 t time to our knowledge, a novel mediator of myeloid cell-IEC crosstalk in maintaining epithelial bar

31 However, how myeloid cell-intrinsic IRF5 regulates the multiple disti

32 one marrow transplantation, and in mice with myeloid cell-specific EGFR deficiency.

33 Unexpectedly, mice without Asxl2 only in myeloid cells (Asxl2DeltaLysM) were completely resistant

34 Genetic deletion of the HIF-2alpha gene in myeloid cells (HIF-2alpha(mye/-) ) markedly exacerbated

35 of heterogeneous cells derived from immature myeloid cells (IMCs).

36 Mice deficient for LKB1 in myeloid cells (LysM-cre x Stk11fl/fl ) or neutrophils (M

37 Brain-resident microglia and myeloid cells (perivascular macrophages) are important H

38 overed that deletion of TGFbeta signaling on myeloid cells (PyMT/TGFbetaRII(LysM)) affects extracellu

39 and soluble triggering receptor expressed on myeloid cells 2 (sTREM2), as well as a marker of neurona

40 variants of triggering receptor expressed on myeloid cells 2 (TREM2) are linked with an enhanced risk

41 a-expressed triggering receptor expressed on myeloid cells 2 (TREM2) gene increase AD risk 2- to 4-fo

42 ia receptor triggering receptor expressed on myeloid cells 2 (TREM2) increase AD risk, and activation

43 iant of the Triggering-Receptor-Expressed on Myeloid cells 2 (TREM2) increases the risk of Alzheimer'

44 Triggering receptor expressed on myeloid cells 2 (TREM2), a receptor exclusively expresse

45 sing TREM2 (triggering receptor expressed on myeloid cells 2) and displaying a fibrosis-promoting phe

46 We discovered that myeloid cells actively engulf invading living Th17 lymph

47 re we show in mice that loss of C9orf72 from myeloid cells alone is sufficient to recapitulate the ag

48 rotein and TREM2-regulated function in human myeloid cells and are the first to show a role for MEK1/

49 ers of brain populating peripherally-derived myeloid cells and endogenous microglia.

50 in the tumor microenvironment (TME) in which myeloid cells and T cells were the most abundant stromal

51 nctions by dampening the interaction between myeloid cells and T cells, orthogonal to PD-1 and other

52 th cis-eQTLs have response eQTLs (reQTLs) in myeloid cells and T cells, respectively.

53 ly expressed in circulating and intratumoral myeloid cells and that high IL8 expression is associated

54 Myeloid cells are a vital component of innate immunity a

55 These myeloid cells are known to secrete several proangiogenic

56 osis and warrants further investigation into myeloid cells as drivers of fibrotic disease.

57 identifies Hyal2-expressing tumor-associated myeloid cells as key players in the accumulation of LMW-

58 ideography to reveal the dynamic behavior of myeloid cells as they interact, extravasate and survey t

59 follows: (1) CH was consistently present in myeloid cells but varied in penetrance in B and T cells;

60 role of the histone deacetylase Hdac3 within myeloid cells demonstrated that Hdac3 promotes M2 activa

61 Myeloid cells derived from bone marrow contribute to the

62 While the magnitude and the phenotypes of myeloid cells diverged between tMCAO and TLR2 stimulatio

63 tion or growth inhibition and a reduction in myeloid cells endogenously expressing high levels of PD-

64 aNKs reduced levels of macrophages and other myeloid cells endogenously expressing high PD-L1 in peri

65 f m(6)A methyltransferase subunit METTL14 in myeloid cells exacerbates macrophage responses to acute

66 expressing lower levels of Mcl and Mincle on myeloid cells exhibited a drastic reduction in EAE incid

67 h was downregulated in both human and murine myeloid cells exposed to LPS as well as other TLR ligand

68 Proinflammatory myeloid cells expressed high levels of CYP27B1 compared

69 n(+) mesenchymal cells expressing CXCL12 and myeloid cells expressing CXCL12 receptor CXCR4.

70 Overall, myeloid cells from anti-41BB-treated tumors had an impro

71 ippocampus with macrophages and inflammatory myeloid cells from the periphery, along with elevated fr

72 , whereas mutation of REVERBalpha in club or myeloid cells had no effect on the bleomycin phenotype.

73 ivery of immunomodulatory compounds to tumor myeloid cells in a variety of cancers.

74 d in myeloid-specific enhancers, implicating myeloid cells in AD etiology.

75 ation, we can delineate biological roles for myeloid cells in different cytokine environments during

76 The critical role of suppressive myeloid cells in immune regulation has come to the foref

77 Depleting CD4 T cells led to increased myeloid cells in peripheral blood, spleen, and bone marr

78 To study the role of myeloid cells in the central nervous system (CNS) in the

79 Microglia are the resident myeloid cells in the central nervous system (CNS).

80 Myeloid cells included 2 populations of proinflammatory

81 Myeloid cells interact with intestinal epithelial cells

82 In addition, IL-33 signaling in myeloid cells is crucial for airway inflammation.

83 e immunity, induced via modulation of mature myeloid cells or their bone marrow progenitors, mediates

84 Both CD4(+) T cells and myeloid cells produced pathogenic levels of VEGF-A withi

85 alpha-dependent factor(s) which regulate the myeloid cells proliferation.

86 recruitment to sites of injury or pathology, myeloid cells represent therapeutic targets for a broad

87 Hence, by dissecting how different myeloid cells respond to cytokine activation, we can del

88 However, it is unknown whether innate myeloid cells retain memory of prior antigenic stimulati

89 lncRNA LUCAT1 which is upregulated in human myeloid cells stimulated with lipopolysaccharide and oth

90 Two myeloid cells subsets.

91 receptor CD200R which is highly expressed on myeloid cells such as macrophages and neutrophils.

92 SCs, and its deletion transformed MDSCs into myeloid cells that activated CD8(+) T cell-mediated immu

93 ) are a heterogeneous population of immature myeloid cells that proliferate in the setting of cancer

94 10 from effector T cells signals to CD11c(+) myeloid cells to suppress an atypical and pathogenic IFN

95 TLR2 agonist rapidly recruited myeloid cells to the CP, increased leukocytosis in the C

96 tibodies or conditional depletion of Insr in myeloid cells using the Cre-loxP system protects mice fr

97 The proliferation of myeloid cells was further promoted by osteocytes lacking

98 y, selective abrogation of EGFR signaling in myeloid cells was sufficient to protect against nephriti

99 B, T, and myeloid cells were analyzed before anti-CD20 administrat

100 Gene networks enriched for myeloid cells were anticorrelated with IL-15 treatment a

101 Overall, not T cells, but myeloid cells were most strongly enriched in AD, and we

102 Myeloid cells were normal in number and function.

103 pply of bone marrow-derived brain-engrafting myeloid cells with donor wild-type CSF1R to repopulate t

104 itch of IL6 signaling from a canonical mode (myeloid cells) to a noncanonical trans-signaling mode (a

105 of HA-degrading activity of Hyal2-expressing myeloid cells, as the engagement of CD44 receptor with s

106 mobilizes immune-suppressive and angiogenic myeloid cells, emerging studies reveal that IL-17 can di

107 Trained immunity, a functional state of myeloid cells, has been proposed as a compelling immune-

108 ther, we show that microglia, not peripheral myeloid cells, release IL-1alpha ex vivo.

109 ompounds with known pharmacology using human myeloid cells, searching for those that enhance TREM2 pr

110 Our results demonstrate that myeloid cells, specifically cells of the nonclassical mo

111 ate and adaptive immune responses that prime myeloid cells, such as macrophages, protect against path

112 ion to IL-10's classic inhibitory effects on myeloid cells, we also describe the nonclassic roles att

113 It is also well-expressed by myeloid cells, where its role is unknown.

114 AD risk genes are specifically expressed in myeloid cells, whereas others are ubiquitously expressed

115 taplegic homolog 7 (SMAD7) in CD34(+)PRLR(+) myeloid cells, which reduced the production of transform

116 tal cells, which are analogous to vertebrate myeloid cells, yet molecular underpinnings of the lymph

117 mia by invading and replicating in mammalian myeloid cells.

118 ognition receptor (PRR)-induced cytokines in myeloid cells.

119 self-renewal, and proliferation of immature myeloid cells.

120 ppressive function of bone marrow Ly6C(high) myeloid cells.

121 ion of VDR in intestinal epithelial cells or myeloid cells.

122 amine the role of IL-33 and ST2 signaling in myeloid cells.

123 ccompanied by an infiltration of T cells and myeloid cells.

124 levels of CYP27B1 compared with homeostatic myeloid cells.

125 Our in vivo studies revealed that myeloid-CITED2 deficiency significantly heightened macro

126 cells (cDC1s) rarely found within the tumor myeloid compartment are crucial for effector T cell recr

127 rostates harvested from mice lacking HO-1 in myeloid compartment.

128 gly, neurodegeneration was not alleviated in myeloid conditional KOs.

129 Leukemic cells, but not their normal myeloid counterparts, depended on the aldehyde dehydroge

130 ubsets, such as CD141+CD11c+ and CD1c+CD11c+ myeloid DCs, distribute throughout several organs in HIS

131 cells were observed in most CD11c(+)CD103(+) myeloid dendritic cells migrating to mediastinal drainin

132 filing, functional assays, and acute in vivo myeloid-depletion experiments identify activation of IGF

133 nd simultaneously decrease the population of myeloid derived suppressor cells (MDSCs) within the tumo

134 Thus, we show that myeloid-derived IL-33 functionally restrains colitic dis

135 promoted M2-like macrophage polarization and myeloid-derived suppressor cell differentiation, respect

136 ls, increases the number of granulocyte-like myeloid-derived suppressor cells (and their expression o

137 Granulocytic myeloid-derived suppressor cells (G-MDSCs) promote tumor

138 Prominent among immunosuppressive cells are myeloid-derived suppressor cells (MDSC) and tumor-associ

139 Myeloid-derived suppressor cells (MDSCs) are a group of

140 Myeloid-derived suppressor cells (MDSCs) are a heterogen

141 Myeloid-derived suppressor cells (MDSCs) are immune cell

142 Myeloid-derived suppressor cells (MDSCs) are immunosuppr

143 As myeloid-derived suppressor cells (MDSCs) are potent immu

144 me to the forefront in cancer research, with myeloid-derived suppressor cells (MDSCs) as a main oncol

145 ced by tumors, neutrophils, and granulocytic myeloid-derived suppressor cells (MDSCs) from cancer pat

146 Myeloid-derived suppressor cells (MDSCs) increase in pat

147 immunoinhibitory actions of tumor-associated myeloid-derived suppressor cells (tumor-MDSCs).

148 ted kinase pathway inhibition and to inhibit myeloid-derived suppressor cells in various melanoma mod

149 angiogenic switching appears to be caused by myeloid-derived suppressor cells recruited to the premet

150 en involve superenhancers of genes active in myeloid development (eg, CD164, PROM1, CDK6, or MYC).

151 reased lymphoid output with a skewing toward myeloid development, and increased memory T cells at the

152 scriptional repression of genes critical for myeloid differentiation and maturation.

153 host receptors like the Toll-like receptor 4/myeloid differentiation factor 2 complex (TLR4/MD-2), mo

154 However, a role for CBFA2T3 in myeloid differentiation of AML has not been reported.

155 s have acquired an oncogenic mutation in the myeloid differentiation primary response 88 (MYD88) gene

156 lity group box 1, nuclear factor kappa beta, myeloid differentiation primary response 88, interferon

157 current DNA copy gains in leukemia, controls myeloid differentiation.

158 d-specific genes in a manner correlated with myeloid differentiation.

159 eved full (>95%) vs low-level (5%-49%) donor myeloid engraftment.

160 but are regulated by AD risk variants within myeloid enhancers in a cell type-specific manner.

161 bility occurring rapidly across thousands of myeloid enhancers in a monocyte-to-macrophage cell fate

162 ed broader rescue of SE-induced effects than myeloid EP2 ablation, including neuroprotection and broa

163 Additionally, br-met-associated CNS-myeloid exhibited downregulation of Cx3cr1.

164 r MASCOT model revealed a dynamic shift from myeloid expansion to lymphoid expansion and subsequent d

165 , it redefines the chromatin topology of the myeloid genome toward a more condensed configuration in

166 Bone marrow (BM) from the sick mice showed myeloid hyperplasia with predominant mature neutrophils,

167 s elicit distinct cytokine profiles by human myeloid immune cells, which are dependent on FcgammaR ac

168 sponses; juvenile mice displayed a sustained myeloid infiltrate (including monocytes and neutrophils)

169 cDC1, and DC2 trajectories, while the common myeloid IRF8(lo) pathway, expressing SIRPA, formed DC3s

170 Finally, overexpression of myeloid KLF2 protects mice from HFD-induced obesity and

171 Our in vivo studies revealed that myeloid-KLF6-deficient mice were highly resistant to end

172 Here, we identify myeloid Kruppel-like factor 2 (KLF2) as an essential reg

173 Paediatric acute myeloid leukaemia (AML) is a heterogeneous disease chara

174 observed in about 35% of patients with acute myeloid leukaemia (AML).

175 and clinical outcome in patients with Acute Myeloid Leukaemia (AML).

176 iac arrest (one [1%]), therapy-related acute myeloid leukaemia (two [3%]), and haematopoietic stem-ce

177 k karyotype, the presence of secondary acute myeloid leukaemia arising from previous myelodysplastic

178 d data on myelodysplastic syndrome and acute myeloid leukaemia cases from ClinicalTrials.gov.

179 ligible patients were 18-70 years, had acute myeloid leukaemia in first or consecutive complete haema

180 ndrome and myelodysplastic syndrome or acute myeloid leukaemia owing to both therapy-resistant diseas

181 r children with relapsed or refractory acute myeloid leukaemia remain poor.

182 s with heavily relapsed and refractory acute myeloid leukaemia suggests that this combination should

183 ible patients had previously untreated acute myeloid leukaemia, an Eastern Cooperative Oncology Group

184 plasm, the presence of therapy-related acute myeloid leukaemia, or being 65 years or older.

185 sed paediatric patients with high-risk acute myeloid leukaemia.

186 ars (95% CI 0.2-2.4) for patients with acute myeloid leukaemia.

187 onse mechanisms underlies the development of myeloid leukaemia.

188 associated with an aggressive form of acute myeloid leukemia (AML) and poor survival rate.

189 Primary acute myeloid leukemia (AML) cells harvested from patients wit

190 performed detailed genetic studies in acute myeloid leukemia (AML) cells.

191 y patients most suitable for intensive acute myeloid leukemia (AML) chemotherapy.

192 epitranscriptome that are required for acute myeloid leukemia (AML) development.

193 Patients with acute myeloid leukemia (AML) harboring FLT3 internal tandem du

194 rent objectives regarding treatment of acute myeloid leukemia (AML) include achieving complete remiss

195 Acute myeloid leukemia (AML) is a cancer derived from the myel

196 Acute myeloid leukemia (AML) is a deadly hematologic malignanc

197 Acute myeloid leukemia (AML) is an attractive system for inves

198 Acute myeloid leukemia (AML) is characterised by a series of g

199 Epigenetic reprogramming in Acute Myeloid Leukemia (AML) leads to the aberrant activation

200 Using acute myeloid leukemia (AML) mouse models, we show AML blasts

201 iously shown that the highly prevalent acute myeloid leukemia (AML) mutation, Arg882His, in DNMT3A di

202 We tested MASQ in a pilot study in acute myeloid leukemia (AML) patients who entered complete rem

203 pathologically relevant event in human acute myeloid leukemia (AML) that contributes to impaired diff

204 nsfusion-independence in patients with acute myeloid leukemia (AML) treated with the isocitrate dehyd

205 of treatment failure for patients with acute myeloid leukemia (AML) who undergo allogeneic stem cell

206 Acute myeloid leukemia (AML) with mixed lineage leukemia 1 (ML

207 eration during leukemogenesis of human acute myeloid leukemia (AML), and ALKBH5 is required for maint

208 e examples, we present our results for acute myeloid leukemia (AML), breast cancer and prostate cance

209 tor venetoclax has an emerging role in acute myeloid leukemia (AML), with promising response rates in

210 o infectious outcomes in patients with acute myeloid leukemia (AML).

211 ost frequent chromosome aberrations in acute myeloid leukemia (AML).

212 treatment-naive elderly patients with acute myeloid leukemia (AML).

213 (LSC) pool determine aggressiveness of acute myeloid leukemia (AML).

214 ly associated with a poor prognosis in acute myeloid leukemia (AML).

215 for Runx1 in a mouse model of inv(16) acute myeloid leukemia (AML).

216 d for treatment of IDH1-mutant (mIDH1) acute myeloid leukemia (AML).

217 nly both over-expressed and mutated in acute myeloid leukemia (AML).

218 een using Msi2-reporter blast crisis chronic myeloid leukemia (bcCML) and identify several adhesion m

219 tween normal and cancerous states in chronic myeloid leukemia (CML).

220 rom the German Study Alliance Leukemia-Acute Myeloid Leukemia (SAL-AML) registry.

221 bl) is a driver oncogene that causes chronic myeloid leukemia and a subset of acute lymphoid leukemia

222 n receiving intensive chemotherapy for acute myeloid leukemia and relapsed acute lymphoblastic leukem

223 th our observations in mice, patient-derived myeloid leukemia cells exhibit KRAS/RAC1/ROS/NLRP3/IL-1b

224 Using The Cancer Genome Atlas acute myeloid leukemia data set, we found an inverse correlati

225 Several acute myeloid leukemia genetic sub-types converge on high expr

226 Acute myeloid leukemia is characterized by the accumulation of

227 ic stressors in the evolution of CH to acute myeloid leukemia or myelodysplastic syndrome.

228 n of m(6)A demethylase ALKBH5 in maintaining myeloid leukemia stem cells.

229 In a xenograft model of acute myeloid leukemia, a single injection of 10 million Jurka

230 with emerging therapeutic potential in acute myeloid leukemia, debilitating fibroses, and obesity-rel

231 epticemia) during remission, and 1 secondary myeloid leukemia.

232 nd that the kinase TTK is important in acute myeloid leukemia.

233 eted or expressed at reduced levels in human myeloid leukemia.

234 Secondary acute myeloid leukemias (AMLs) evolving from an antecedent mye

235 al heterogeneity is a common feature of many myeloid leukemias and a significant reason for treatment

236 3a2 was seen across multiple mouse and human myeloid leukemias.

237 HSCT while maintaining lifelong infection in myeloid lineage cells.

238 of obesity, we explored the role of ASXL2 in myeloid lineage cells.

239 , arguing against a direct role for CSF1R in myeloid lineage commitment.

240 We first establish the essential role of the myeloid lineage for tail regeneration in the regeneratio

241 leukemia (AML) is a cancer derived from the myeloid lineage of blood cells, characterized by overpro

242 he effects of differential activation of the myeloid lineage on the creation of a regeneration-permis

243 latency, and their differentiation along the myeloid lineage triggers cellular cues that drive reacti

244 poles with immune-suppressing drugs restores myeloid lineage-controlled cellular mechanisms.

245 pluripotent stem cells was skewed toward the myeloid lineage.

246 ylation signatures are more prominent in the myeloid lineage.

247 ine in lymphopoiesis and skewing towards the myeloid lineage.

248 These CD34(+)PRLR(+) myeloid-lineage progenitors were derived from granulocyt

249 miR-223 restricts the EHT of lymphoid-myeloid lineages by suppressing the mannosyltransferase

250 Myeloid LKB1 deficiency was associated with reduced cyto

251 s (platelets, mature/immature red cells, and myeloid/lymphoid/compound white cells) and 49 haemostasi

252 thus uncovers T cell recognition of HERVs in myeloid malignancies, thereby implicating HERVs as poten

253 man-Diamond syndrome before development of a myeloid malignancy and could have been monitored with bo

254 ease the risk of transformation from CH to a myeloid malignancy.

255 atopoiesis and increased risk for developing myeloid malignancy.

256 e, preceding development of aging-associated myeloid malignancy.

257 l (HSC) function, and increased incidence of myeloid malignancy.

258 tivation of IGF1R as a critical component of myeloid-mediated T-ALL growth and survival.

259 tic issues in the 2017 WHO classification of myeloid neoplasms and the importance of NPM1 mutations i

260 nd RUNX1 mutations such as histiocytoses and myeloid neoplasms.

261 her bone marrow (BM)-resident or circulating myeloid OC progenitors (OCP) expressing the receptor CX(

262 ncy, GM-CSF deficiency, or modulation of the myeloid population through clodronate-mediated depletion

263 ceptor TIGIT and the deletion of suppressive myeloid populations appear attractive, particularly afte

264 ed MerTK mRNA and protein expression in both myeloid populations, resulting in reduced capacity of th

265 imary bone marrow revealing perturbed UPR in myeloid precursors and in vitro differentiation of prima

266 SCs gave rise to megakaryocytic-erythroid or myeloid precursors.

267 Using Kasumi-3 cells as a myeloid progenitor cell model endogenously expressing MH

268 driver mutation is present in a BM-resident myeloid progenitor that can be mobilized to the blood.

269 Importantly, the abnormal myeloid progenitors (AMPs), a leukemia-initiating cell p

270 opoietic-stem-cell (HSC)-independent erythro-myeloid progenitors (EMPs) present in the murine yolk sa

271 Conditional deletion of Hdac3 within myeloid progenitors accelerates healing of cortical bone

272 al changes may promote expansion of abnormal myeloid progenitors in del(5q) MDS, and in rare cases dr

273 ient induction requires direct engagement of myeloid progenitors in the bone marrow.

274 Moreover, CD34(+)PRLR(+) myeloid progenitors lacked lymphoid developmental potent

275 ere we aimed to investigate the influence of myeloid progenitors on CD34(+) cell differentiation into

276 ene expression analysis of mirn23a-deficient myeloid progenitors revealed a decrease in TLR and IFN s

277 which requires maintenance and expansion of myeloid progenitors.

278 TREM2 is a myeloid receptor that transmits intracellular signals th

279 ur results uncover a mechanism that controls myeloid regeneration and early lineage decisions in HSCs

280 Notch and Wnt signaling transiently triggers myeloid regeneration from HSCs in response to stress, an

281 asms (MDSs/MPNs) harbor somatic mutations in myeloid-related genes, but still, current diagnostic cri

282 phosphatase-interacting protein 1-associated myeloid-related proteinemia inflammatory (PAMI) syndrome

283 en were observed during acute infection with myeloid-restricted ZIKV that precluded the generation of

284 ges in HSCs that occur in old age, including myeloid skewing, reduced reconstitution potential, impai

285 trated that AD risk variants are enriched in myeloid-specific enhancers, implicating myeloid cells in

286 Mice with myeloid-specific gene deletion of Traf3ip3 have increase

287 n spontaneous and ATRA-induced activation of myeloid-specific genes in a manner correlated with myelo

288 y insertion of a complementary sequence to a myeloid-specific microRNA in the 3' untranslated region.

289 tic depletion of either Tlr4 (Tlr4(-/-) ) or myeloid-specific Tlr4 (Tlr4(f/f)Lyz2(Cre+)) resulted in

290 I-associated interaction domains, interrupts myeloid-specific transcription factors binding at enhanc

291 Myeloid-specific Wnt5A knockdown also led to decreased l

292 Myeloid-specific, IL-33-deficient or ST2-deficient mice

293 Our comprehensive analysis of key myeloid subsets in human and mouse identifies critical c

294 e highest constitutive levels of BAFF; other myeloid subsets, including conventional dendritic cells

295 r immunity and defines mechanisms underlying myeloid-targeted immunotherapies currently undergoing cl

296 CTCF binding was enriched for motifs for key myeloid transcription factors such as CEBPA, PU.1, and R

297 gs provide insights into the pathogenesis of myeloid transformation and how clonal complexity evolves

298 (CBFA2T3, also known as MTG16 or ETO2) is a myeloid translocation gene family protein that functions

299 sults demonstrate that loss of Cx3cr1 in CNS-myeloid triggers a Cxcl10-mediated vicious cycle, cultiv

300 reconstruction of the epithelial-mesenchymal-myeloid unit of the distal lung, thereby opening numerou

301 icient mice were used to compare the role of myeloid- versus intestinal epithelial cell-derived IL-33