ライフサイエンスコーパス: macrophage

1 okine and chemokine expression in intrarenal macrophages.

2 ed pro-inflammatory gene expression in THP-1 macrophages.

3 tioned medium derived from HCV-exposed human macrophages.

4 1beta up-regulated the expression of HCA2 on macrophages.

5 is were partially dependent upon T cells and macrophages.

6 , MCP-1, IL-1, IL-6, ICAM-1, VCAM-1 and CD68 macrophages.

7 l cells, similar to the behavior observed in macrophages.

8 receptor (LXR)alpha in lung fibroblasts and macrophages.

9 ymes allowing the control of phagocytosis in macrophages.

10 in were similar in MSK1/2 and DUSP1 knockout macrophages.

11 athepsin K compared with resting unpolarized macrophages.

12 cytic activity of pro- and anti-inflammatory macrophages.

13 lation of TAK1 triggers spontaneous death in macrophages.

14 neutrophils and to ERV-1/ChemR23 on monocyte/macrophages.

15 ncreases pro-interleukin-1beta expression in macrophages.

16 survival of the parasite within the infected macrophages.

17 rs of cells underwent differentiation toward macrophages.

18 secretion during L. pneumophila infection of macrophages.

19 ablishment of persistent infection in tissue macrophages.

20 l growth with very low toxicity towards host macrophages.

21 m vacuoles and inhibits Salmonella growth in macrophages.

22 beta by inhibiting the NLRP3 inflammasome in macrophages.

23 fection outcomes in individual primary human macrophages.

24 ption 1 signaling and dsRNA viral sensors in macrophages.

25 pathway to mTOR to induce autophagy in host macrophages.

26 d in cells of the myeloid lineage, including macrophages.

27 rough the recruitment and subversion of host macrophages.

28 d phagocytosis of Staphylococcus aureus into macrophages.

29 n in lipid deposition in aortas and isolated macrophages.

30 be the most pertinent mediator of increased macrophages.

31 occurred in dendritic cells (DCs) but not in macrophages.

32 rosis, due to its active uptake by monocytes/macrophages.

33 2 marker Arginase 1 in inflammatory-elicited macrophages.

34 mpairs the replication of M. bovis in bovine macrophages.

35 own with small hairpin RNAs in human primary macrophages.

36 he predominant BCAT isoform in human primary macrophages.

37 which impairs the antibacterial response of macrophages.

38 ssociated antigen 1 (LFA-1) (CD11a/CD18) and macrophage-1 antigen (CD11b/CD18).

39 Leishmania replicates intracellularly in macrophages, a process that is essential for disease pro

40 However, macrophage ability to produce nitric oxide was defective

41 together with disturbed proportion of M1/M2 macrophages, accompanied by enhanced formation of arteri

42 ggested that CCL5, secreted from HCV-exposed macrophages, activates inflammasome and fibrosis markers

43 se data show that VSIG4 negatively regulates macrophage activation by reprogramming mitochondrial pyr

44 Pro-tumorigenic M2 macrophage activation was diminished in myeloid-specific

45 infection, LipA suppresses pro-inflammatory macrophage activation, rendering these cells inefficient

46 e involved in the physiological cessation of macrophage activation.

47 e the collateral destruction associated with macrophage activation.

48 , from hematopoiesis to monocyte changes and macrophage activation.

49 the effect of therapies targeting microglia/macrophages activation after TBI.

50 Islet beta-cell dysfunction and aggressive macrophage activity are early features in the pathogenes

51 These data suggest that replication in macrophages affects cellular function and plays an impor

52 enetic deletion of monocyte-derived alveolar macrophages after their recruitment to the lung ameliora

53 Toll-like receptors in alveolar macrophages (AMPhi) recognize the molecular constituents

54 equired direct adhesive interactions between macrophages and adipocytes mediated by the integrin alph

55 ammation and glucose metabolism by targeting macrophages and adipocytes, respectively.

56 ing by C. albicans The peptide also protects macrophages and augments their antifungal activity.

57 cytokine expression and bacterial killing in macrophages and boosted protection against intravenous b

58 their ability to induce cytokine response in macrophages and cardiomyocytes.

59 ns Tat or gp120 induces TREM-1 expression in macrophages and confers anti-apoptotic attributes.NF-kap

60 in infection, causing iron sequestration in macrophages and decreased plasma iron; this is proposed

61 Mycobacterium tuberculosis-infected macrophages and dendritic cells are limited in their abi

62 We confirmed (68)Ga-DOTATATE binding in macrophages and excised carotid plaques.

63 matory niches consisting of tumor-associated macrophages and fibroblasts contribute to treatment tole

64 2-driven activation of NLRP3 inflammasome in macrophages and indicates a potential host-directed ther

65 Here, we analyzed CB1R signaling in macrophages and its developmental role in T2D.

66 Finally, in vitro IH exposures of murine macrophages and LLC1 cells showed that both cell types i

67 reased accumulation of inflammatory monocyte macrophages and neutrophils in the lungs of male mice, a

68 Leukocytes composed mainly of macrophages and neutrophils infiltrate infected DRGs and

69 bacterial surface, promoted phagocytosis by macrophages and neutrophils, and protected mice from MRS

70 ic activity, enhancing parasite clearance by macrophages and neutrophils.

71 pressed in wound-infiltrated neutrophils and macrophages and play central roles in wound healing.

72 hus, c-Jun regulates the activation state of macrophages and promotes arthritis via differentially re

73 axis elevates intratumoral Tregs and M2-like macrophages and reduces CD8+ T cells to promote lung tum

74 les, and full renal protection required both macrophages and renal tubular cells.

75 However, unlike tissue macrophages and similar to DCs, they homeostatically mig

76 Finally, selective killing of Mtb-infected macrophages and subsequent bacterial release enabled rif

77 that [(64)Cu]-LLP2A retention was driven by macrophages and T cells, with less contribution from neu

78 IL-10-mediated suppression in LPS-stimulated macrophages and that inhibited genes can be divided into

79 s alternative activation of tumor-associated macrophages and the growth of colon cancer xenografts.

80 mpaired the proliferation of tissue-resident macrophages and the induction of anti-inflammatory and t

81 itates both their direct priming by resident macrophages and the localized delivery of innate signals

82 In the present study, we hypothesized that macrophages and their M1/M2 activation critically involv

83 than 90% necrotic material admixed with few macrophages and viable cells at their outer rim.

84 cking one SODA allele failed to replicate in macrophages and were severely attenuated in their abilit

85 T lymphocytes and classic M1 proinflammatory macrophages) and decreased expression levels of proinfla

86 ion in fibrocytes (possibly including tissue macrophages) and T and B lymphocytes in the presence of

87 d crescent formation and abrogated monocyte, macrophage, and dendritic cell increase in the affected

88 e resulted from a genuine effect of Trpc3 on macrophages, and (b) whether the reduced necrosis and ma

89 Activated and memory CD4 T cells, macrophages, and dendritic cell (DC) showed chemoattract

90 tion may go hand-in-hand with necroptosis in macrophages, and revises current understanding of indepe

91 summary, C. neoformans harvests lipids from macrophages, and the C. neoformans-macrophage interactio

92 These observations demonstrate that Ly6C(+) macrophage apoptosis and decreased ingress of circulatin

93 es, and (b) whether the reduced necrosis and macrophage apoptosis in plaques of these mice was a mani

94 The ability to suppress host macrophage apoptosis is essential for M. tuberculosis (M

95 ole in pathogenesis during infection in vivo Macrophages are a critical first line of defense against

96 Whether monocytes and macrophages are equipped with an allorecognition system

97 ip as a mammalian model, we demonstrate that macrophages are essential for the regeneration process.

98 Marrow-derived macrophages are highly phagocytic, but whether they can

99 Macrophages are prominent immune cells in the tumor micr

100 Polarization is not fixed, as macrophages are sufficiently plastic to integrate multip

101 d serum sCD163 levels (a marker of activated macrophages) are greater in individuals with the IFNL3-I

102 tective phenotype involved the clustering of macrophages around S1 segments of proximal tubules, and

103 h inflammatory monocytes and tissue-resident macrophages as sources of TAMs.

104 4b (GS-5734) with anti-EBOV EC50 = 86 nM in macrophages as the clinical candidate.

105 th only, or both intracellularly on infected macrophages as well as extracellularly on bacterial grow

106 In myeloid-derived dendritic cells and macrophages as well as resting T-cells, SAMHD1 blocks HI

107 Up to now, AT macrophages (ATM) accumulation was considered to be due

108 found that after infection, a population of macrophages became necrotic, providing a niche for M. tu

109 nd primary PHD2 knockout bone marrow-derived macrophages (BMDM).

110 /beta, NF-kappaB p65) in bone marrow-derived macrophages (BMDMs) from knockout mice.

111 l Bmp6 knockout mice, whereas hepatocyte and macrophage Bmp6 conditional knockout mice exhibited no i

112 T lymphocytes and macrophages both display immunosuppressive characteristi

113 he adipose tissue and expansion of activated macrophages, both of which occurred prior to changes in

114 1 mAb supported the pathogenic role of these macrophages but not the PD-L1(-) PMN in GN development a

115 undergo apoptosis before they are removed by macrophages, but if apoptosis is delayed, neutrophils ca

116 optotic cells, or efferocytosis, by lesional macrophages, but the mechanisms underlying defective eff

117 colon mesenchymal cells (CMCs) generated M2 macrophages by regulating their shape during recovery.

118 hese events were linked to a decrease in the macrophage capacity for NTHi phagocytosis and increased

119 Small alveolar macrophage CD206 expression was lower in COPD patients c

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

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

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

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

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

125 ifferentiation and behavior and describe how macrophages change during protective immunity and inflam

126 gulation of macrophage glucose metabolism by macrophage colony-stimulating factor (M-CSF; inflammatio

127 ired high langerin and CD1a with granulocyte-macrophage colony-stimulating factor and transforming gr

128 lease of miR-21 contribute to sensory neuron-macrophage communication after damage to the peripheral

129 amined its regulation and function in murine macrophages, compared it to the LD adipose differentiati

130 d proinflammatory gene expression and plaque macrophage content.

131 n, and activation of alternatively activated macrophages, contributed by deregulation of the miR-155

132 M1), and anti- (CD206(+) = M2) inflammatory macrophages, crown-like structures, and senescent cells,

133 In the presence of C3, macrophage death was observed at 24 h postinfection in a

134 CD11d-deficient M1 macrophages demonstrated improved migration in a three-d

135 L-6, IL-8, CD38, and CD69 and down-regulated macrophage-derived chemokine, human leukocyte antigen DR

136 h a cytokine-signaling network that involves macrophage-derived IL-1beta and fibroblast-derived CXCR2

137 g fibrosis, whereas tissue-resident alveolar macrophages did not contribute to fibrosis.

138 In diabetes, macrophages display a prolonged inflammatory phenotype i

139 us, we conclude that alternatively activated macrophages do not synthesize relevant amounts of catech

140 expressed by mouse monocyte-derived alveolar macrophages during fibrosis were up-regulated in human a

141 e have previously shown that ACKR2 regulates macrophage dynamics during lymphatic vessel development.

142 Regulation of macrophage dynamics during these processes can therefore

143 evidence was identified to support a role of macrophage efflux to draining lymph nodes following trea

144 ng, and increased number of pro-inflammatory macrophages emerged in VWAT along with 1520 DMRs (P < 0.

145 er, our results reveal new insights into how macrophages enhance cancer cell metastasis, and they ide

146 Bim-deleted kidney macrophages exhibit a novel transcriptional lupus signat

147 Macrophages exhibit phenotypic plasticity, as they have

148 TET2-deficient macrophages exhibited an increase in NLRP3 inflammasome-

149 Together, our results demonstrate that human macrophages exposed to HCV induce CCL5 secretion, which

150 TREM-1 silencing in macrophages exposed to HIV-related proteins led to incre

151 q-Well to profile thousands of primary human macrophages exposed to Mycobacterium tuberculosis.

152 lls is necessary for proper tumor-associated macrophage expression of IFNgamma-inducible genes.

153 iography and compared with CXCR4 and RAM-11 (macrophage) expression on adjacent histologic sections.

154 reactivity, and reduced expression levels of macrophage factors that are associated with resolution o

155 We found that PRMT1 knock-out macrophages failed to up-regulate PPARgamma expression i

156 are responsible for the initial reduction of macrophages following infliximab treatment in hTNF-Tg mi

157 ced higher TNF-alpha compared with CD44(-/-) macrophages following TLR2 stimulation (p < 0.01).

158 Exposure to BAR501 shifted intestinal macrophages from a classically activated (CD11b(+), CCR7

159 Macrophages from Cmah(-/-) mice secreted more inflammato

160 Alveolar macrophages from female mice exhibited greater expressio

161 Furthermore, IL-4-stimulated macrophages from female mice exhibited more transcriptio

162 fibrosis were up-regulated in human alveolar macrophages from fibrotic compared with normal lungs.

163 d estrogen receptor (ER) alpha compared with macrophages from male mice following allergen challenge.

164 modifications at M2 gene promoters than did macrophages from male mice.

165 trogen are long-lasting; bone marrow-derived macrophages from ovariectomized mice implanted with estr

166 L-4-induced M2 gene expression compared with macrophages from placebo-implanted littermates.

167 IL-10-mediated negative feedback control of macrophage function in vitro However, the in vivo effect

168 , understanding how viruses evade or exploit macrophage function will provide greater insight into vi

169 lts establish a regulatory role for BCAT1 in macrophage function with therapeutic implications for in

170 iral life cycle or productive replication on macrophage function, we assessed cytotoxicity, nitric ox

171 hypothesized that differential regulation of macrophage glucose metabolism by macrophage colony-stimu

172 onnexin-43-containing gap junctions, cardiac macrophages have a negative resting membrane potential a

173 Macrophages have important functional roles in regulatin

174 BM components require secretion by migrating macrophages (hemocytes) during their developmental dispe

175 l-type-specific anti-inflammatory effects on macrophages, hepatocytes, and adipocytes, which is disti

176 Dectin-1 is specifically recruited to the macrophage-hyphal interface but not the macrophage-spore

177 We conclude that ESAT-6 stimulates macrophage IL-6 production through STAT3 activation.

178 CXCL9 expression in lesional macrophages implicates the skin as the source of circula

179 phagocytosing cells of the CNS, and invading macrophages in degenerative and regenerative processes a

180 Together, M2-like macrophages in fibrotic liver exert the protective effec

181 ted in an increased total number of lesional macrophages in general and Ly6c(hi) infiltrating monocyt

182 Our findings define a role for mTORC2 in macrophages in integrating signals from the immune micro

183 f PD-L1 by CD11b(+)F4/80(-)I-A(-) glomerular macrophages in kidneys of mice with GN and the inhibitio

184 n general and Ly6c(hi) infiltrating monocyte-macrophages in particular, accompanied by skewed M2 to M

185 We discuss the properties of macrophages in steady-state barrier tissues, outline the

186 new foundational role for CXCR3(+) monocytes/macrophages in the process of tumor engraftment in the l

187 st time the involvement of TLRs expressed on macrophages in the recognition of and response to Acanth

188 g the immune response toward either M1 or M2 macrophages in vivo, wild-type mice were injected with g

189 ked metabolic changes in the Irgm1-deficient macrophages, including increased glycolysis and an accum

190 M1- but not M2-polarized macrophages induced EndMT in ECs.

191 STING cytosolic sensing pathway in resident macrophages, inducing the production of the chemokine CC

192 In vitro, CD44TA-SMP accumulated in macrophages infected with mycobacteria efficiently killi

193 The same effect of macrophage infiltrate on EGFR activation was also seen i

194 inly by immunomodulation, which led to lower macrophage infiltration and higher presence of regulator

195 Finally, macrophage infiltration and target:background ratio were

196 ed by evidence of adipocyte death, increased macrophage infiltration, and tissue fibrosis.

197 rulonephritis in rats, in part by decreasing macrophage infiltration.

198 terleukin-6, interleukin-13, interleukin-17, macrophage inflammatory proteins-1alpha, and macrophage

199 macrophage inflammatory proteins-1alpha, and macrophage inflammatory proteins-1beta) when CD73 was la

200 viously unidentified role for peroxisomes in macrophage inflammatory responses and suggest that perox

201 pids from macrophages, and the C. neoformans-macrophage interaction is modulated by exogenous lipids,

202 phenotypic conversion of F4/80(int)CD206(+) macrophages into F4/80(hi)CD206(-) macrophages was assoc

203 sette stability and is sufficient to inhibit macrophage invasion.

204 istically distinct phenotypes with regard to macrophage invasion: a defect in matrix degradation, due

205 nstrated that higher numbers of infiltrating macrophage iron deposits was associated with lower anti-

206 arginine and tryptophan by immunoregulatory macrophages is one pathway that suppresses local T cell

207 ROS generation in human CD68(low)CD14(high) macrophages is strongly suppressed by inhibition of dyna

208 Knocking down TTP in primary macrophages leads to an increased induction of NLRP3 by

209 (HEL) cells and beta1 integrin activation in macrophage-like RAW264.1 cells.

210 red a synthetic phenotype, the occurrence of macrophage-like SMCs in the lesions, and impaired choles

211 h a marked tropism for cells of the monocyte-macrophage lineage, affecting swine species and provokin

212 re rapidly with greater angiogenesis and had macrophages localizing to the tumor edge which were more

213 er inflammatory response of the encountering macrophages, manifested by elevation in mRNA expression

214 ial-driven expression of IL-19 by intestinal macrophages may contribute to the pathogenesis of inflam

215 mice, a benefit achieved in part by reducing macrophage-mediated injury at the lesion epicenter.

216 Quinolinic acid, a macrophage/microglia-derived excitotoxin fulfills a plet

217 Microarray analysis suggested downregulated macrophage migration inhibitory factor (MIF) to be the m

218 es their distinct roles in the regulation of macrophage migration.

219 us to explore the possibility that resident macrophage/monocyte-like cells in the cochlea can mediat

220 Macrophage motility, phagocytosis, and differentiation i

221 were generated by coculturing primary human macrophages (MPhi) with human MCF-7 breast carcinoma cel

222 ment and adhesive functions of monocytes and macrophages (Mvarphi) and the ability of these cells to

223 ells, dendritic cells (DCs), and residential macrophages near high endothelial venules, the results h

224 h in classically and alternatively polarized macrophages, NFAT5 enhanced functions associated with a

225 ts showing that NLRP1 enhances pyroptosis in macrophages, NLRP1 in melanoma behaved differently in th

226 In SIRT3 knock-out bone marrow-derived macrophages, NLRP3 activation promoted excess cytosolic

227 Thus, the macrophages of the islets of Langerhans are poised to mo

228 Analyses of macrophages on soft (like marrow) or stiff (like solid t

229 mice, and depletion of inflammatory monocyte macrophages partially protected these mice from lethal S

230 ave found that in murine bone marrow-derived macrophages, PGE2 via the cAMP/protein kinase A pathway

231 e of residence defined the core signature of macrophages, phagocytosis imprinted a distinct antiinfla

232 lex, which promotes the anti-inflammatory M2 macrophage phenotype, and assists TRXR1-regulated arrest

233 n particular, accompanied by skewed M2 to M1 macrophage phenotype.

234 1alpha) as a critical switch governing M1-M2 macrophage polarization and energy balance.

235 nges in neutrophil, naive CD4(+) T cell, and macrophage populations during peanut challenge.

236 ymeric cores with cell membrane derived from macrophages, possess an antigenic exterior the same as t

237 ial inflammation, driven by monocyte-derived macrophages, predicts future cardiovascular events in th

238 selective effect of TRPC3 on apoptosis of M1 macrophages previously observed in vitro.

239 POP2 also impairs macrophage priming by inhibiting the activation of non-c

240 questration and destruction via local tissue macrophages, prion trafficking by B and dendritic cells

241 ria monocytogenes, DNA-PKcs-deficient murine macrophages produce reduced levels of IL-18 and are unab

242 CD44(+/+) murine bone marrow-derived macrophages produced higher TNF-alpha compared with CD44

243 -erythroid progenitor (MEP), and granulocyte-macrophage progenitor (GMP) cells, accompanied by increa

244 man sarcoidosis patients, mTORC1 activation, macrophage proliferation and glycolysis were identified

245 MN and plays an important role in regulating macrophage properties during and after engulfment.

246 In cultured macrophages, recombinant CTRP6 dose-dependently up-regul

247 During bacterial infection of macrophages, RECON antagonized STING activation by actin

248 examination, we observed delayed and reduced macrophage recruitment in medaka, along with delayed neu

249 SBs act as signaling intermediates in murine macrophages, regulating innate immune responses through

250 3-infected NOD.Ncf1(m1J) bone marrow-derived macrophages rescued the inflammatory antiviral M1 macrop

251 f Cell, Hulsmans et al. identify a subset of macrophages residing within the cardiac conduction syste

252 phages rescued the inflammatory antiviral M1 macrophage response, revealing reduction-oxidation-depen

253 and promoting the development of reparative macrophage responses.

254 Bmal1 deficiency in monocytes and macrophages resulted in an increased total number of les

255 polarization of human primary monocytes into macrophages results in lower expression and activity of

256 n-mediated CD11d upregulation contributes to macrophage retention at inflammatory sites during athero

257 MK2 positively regulated the following macrophage RNA: Emr1 (F4/80), Itgam (CD11b), Csf1r (M-CS

258 infection, and small interfering RNA treated-macrophages showed reduction in IL-1beta secretion and c

259 Experiments using murine macrophages showed that FPW extract is able to reduce th

260 n vivo upon challenge with allergen and that macrophage-specific deletion of ERalpha impaired this M2

261 the macrophage-hyphal interface but not the macrophage-spore interface due to differences in carbohy

262 Macrophage subpopulation cell-surface expression of immu

263 g of dead cells via receptors present on the macrophage surface results in the translocation of the a

264 ting the formation of an FX reservoir at the macrophage surface.

265 assive accumulation of infiltrated MAC387(+) macrophages, T cells, dendritic cells (DCs), and residen

266 resistance are linked with tumor-associated macrophage (TAM) and myeloid-derived suppressor cell (MD

267 -infiltrating immune cells, tumor-associated macrophages (TAMs) take a center stage in promoting both

268 e well-known limitations of tumor-associated macrophages (TAMs).

269 ed at 24 h postinfection in a quarter of the macrophages that contained only 1 to 5 bacterial cells.

270 20-dependent membrane trafficking pathway in macrophages that maintains Mtb in spacious proteolytic p

271 ight about other molecular signatures within macrophages that might be affected by Trpc3 expression r

272 We examined the transcriptional profiles of macrophages that reside in the islets of Langerhans of 3

273 ies on chemokine/cytokine release from human macrophages, the prostanoid EP1 receptor played a permis

274 overexpression by genetically modified HO-1 macrophage therapy was accompanied by decreased OLT dama

275 ter the hostile oxidative environment inside macrophages, these protozoans contain anti-oxidant syste

276 Like many tissue macrophages, they self-maintain locally.

277 Aging impairs the ability of alveolar macrophages to limit lung damage during influenza infect

278 (2017) reveal that cytoplasmic transfer from macrophages to melanoma cells correlates with melanoma i

279 Tumors routinely attract and co-opt macrophages to promote their growth, angiogenesis, and m

280 responsible for the poor inherent ability of macrophages to respond to chemokine gradients was suppor

281 y compartment-independent activation of lung macrophages toward a conserved hypoxia program, with the

282 ifferentiation of mouse peritoneal and human macrophages toward a proinflammatory M1 phenotype.

283 hielding during irradiation preserves normal macrophage transition dynamics and subsequently muscle t

284 here show that compartmentalized and active macrophage-tropic HIV-1 variants are present in the brai

285 robes, but could also promote infection with macrophage-tropic pathogens.

286 CE The detection of highly compartmentalized macrophage-tropic R5 Envs in the brain tissue of HIV pat

287 The detection of active macrophage-tropic virus expression, and probably replica

288 d evaluated for in vivo absorption, alveolar macrophage uptake, and safety.

289 zole moiety, which physically interacts with macrophages via histamine receptors, exhibits substantia

290 by augmented PV degradation in Wnt5a-treated macrophages was also apparent from transmission electron

291 )CD206(+) macrophages into F4/80(hi)CD206(-) macrophages was associated with almost complete remodeli

292 of DHRS9 within a panel of monocyte-derived macrophages was investigated by quantitative PCR, immuno

293 ammation, whereas migration of CD11b(-/-) M1 macrophages was not affected.

294 fer in proinflammatory and anti-inflammatory macrophages, we compared the macropinocytic ability of t

295 cytokine responses in R753Q TLR2-expressing macrophages were accompanied by impaired phosphorylation

296 P2X7-competent and P2X7-deficient macrophages were isolated and stimulated with lipopolysa

297 Although macrophages were more potent in uptaking tumor DNA, incr

298 initiation of therapy, at which time Ly6C(+) macrophages were significantly reduced in the ankles.

299 h a regulatory or an exhausted phenotype and macrophages with an M2 phenotype.

300 the maintenance of proinflammatory CD11c(+) macrophages within lesions and controlling the expansion