ライフサイエンスコーパス: M1 macrophage

1 el in M-BMM (M2 macrophages) than in GM-BMM (M1 macrophages).

2 iation/polarization toward a proinflammatory M1 macrophage.

3 uding IL-6 and TNF, in human proinflammatory M1 macrophages.

4 phenotype via downregulation of the IL-10 in M1 macrophages.

5 reased transcription from P3 in inflammatory M1 macrophages.

6 ctor IRF5 up-regulates genes associated with M1 macrophages.

7 lammatory cells and also the polarization of M1 macrophages.

8 okines and a higher level of PTPN22 in human M1 macrophages.

9 he maturation of immature myeloid cells into M1 macrophages.

10 both nonpolarized and classically polarized M1 macrophages.

11 (IFN-gamma), which mediated the induction of M1 macrophages.

12 was confirmed using monocyte-derived DC and M1 macrophages.

13 g pathway promoted MDSC differentiation into M1 macrophages.

14 irst few days and initially transformed into M1 macrophages.

15 eby inhibiting the generation of tumoricidal M1 macrophages.

16 ly increasing tumor necrosis factor-alpha in M1 macrophages.

17 CR-associated samples have more inflammatory M1 macrophages.

18 (CXCL1, CXCL5, RANTES) released by activated M1 macrophages.

19 rkers (caspase-1 and NO) only coexpressed by M1 macrophages.

20 macrophages and an increase in tumor-killing M1 macrophages.

21 ne infiltrates, particularly neutrophils and M1 macrophages.

22 that directed macrophage polarization toward M1 macrophages.

23 can promote CKD symptoms via infiltration of M1 macrophages.

24 downregulated in control vs. Trpc3-deficient M1 macrophages.

25 ted infections which contained predominately M1 macrophages.

26 nd with anti-CD163 for M2, and anti-iNOS for M1 macrophages.

27 Moreover, M1 macrophages accumulated in the renal interstitial com

28 d-type counterparts, and obstruction-induced M1 macrophages accumulation and M1 chemokine expression

29 immune-inflamed microenvironment with higher M1 macrophage activation (0.16 vs 0.12; P = .047) and in

30 ctivation within macrophages is required for M1 macrophage activation and anti-C. neoformans activity

31 lar dystrophy that may be caused by reducing M1 macrophage activation and cytotoxicity, increasing M2

32 that Odc deletion in myeloid cells enhances M1 macrophage activation and gastritis.

33 clear leukocytes and macrophages, stimulated M1 macrophage activation and interleukin 10 release, and

34 phage-derived ODC is a critical regulator of M1 macrophage activation during both Helicobacter pylori

35 mmatory feedback loop formed by inflammatory M1 macrophage activation of T-cells as a driving force u

36 in more severe inflammation with an enhanced M1 macrophage activation phenotype.

37 on of an M2-like phenotype in late stages of M1 macrophage activation to promote wound healing.

38 Surprisingly, diminished M1 macrophage activation was also detectable, as marked

39 Basal M1 macrophage activation was characterized by elevated l

40 revealed that genes implicated in classical M1 macrophage activation were stimulated by HCMV infecti

41 response, increased fungal burden, deficient M1 macrophage activation, and loss of protection.

42 ely, VASP deficiency induced proinflammatory M1 macrophage activation, and the transplantation of bon

43 eprogramming of mitochondrial metabolism for M1 macrophage activation.

44 on of genes associated with proinflammatory (M1) macrophage activation and was protective for multipl

45 transcription 1 (STAT1)-mediated classical (M1) macrophage activation.

46 Furthermore, M1 macrophages adapt to a cytokine environment by revers

47 eukin-12 (IL-12), but not IL-10, produced by M1 macrophages also abrogated M1-mediated downregulation

48 SOCS3-deficient M1 macrophages also have a stronger capacity to induce T

49 faecal and colonic microbial growth; reduced M1 macrophage and increased M2 macrophage infiltration i

50 ionally, C3H/HeJ (TLR4 mutant) mice reversed M1 macrophage and TH1/TH17 polarization after TBI compar

51 -alpha(+) and IL-1beta(+) islet-infiltrating M1 macrophages and a concomitant enhancement in arginase

52 stead with a marked increase in the level of M1 macrophages and a requirement for IFNgamma receptor e

53 These nanocells polarize M1 macrophages and activate NK cells concurrently produc

54 nuum between the extremes of proinflammatory M1 macrophages and anti-inflammatory M2 macrophages.

55 e response, but did result in a reduction of M1 macrophages and capsule deposition downstream.

56 ed to detect the expression of CD68(+)CD86(+)M1 macrophages and CD68(+)CD206(+)M2 macrophages.

57 reased infiltration of classically activated M1 macrophages and decreased alternatively activated M2

58 significantly reduced the number of iNOS(+) M1 macrophages and increased the expression of anti-infl

59 ted proinflammatory cytokine production from M1 macrophages and induced a M2-to-M1 polarization switc

60 13 and requires the induction of tumoricidal M1 macrophages and lymphocytes combined with a reduction

61 on in the tumor microenvironment, recruiting M1 macrophages and prolonging survival.

62 Bacterial d-aa stimulate M1 macrophages and promote survival of intestinal naive

63 ated the innate immune system to skew toward M1 macrophages and release inflammatory cytokines in an

64 resistance because IL-4Ralpha(-/-) mice have M1 macrophages and retain high levels of myeloid suppres

65 We found that CD169 labels M1 macrophages and that conditioned medium (CM) from M1

66 synthase expression, indicative of enhanced M1 macrophages and the development of steatosis.

67 on of key mediators of classically activated M1 macrophages and thus of innate immune responses to Li

68 In the current study, we defined "M1" macrophage and "M1"/"M2" ratio by transcriptomic sig

69 t resolved and toward classically activated (M1) macrophages and Th1 cells during disease that progre

70 fatty acids within inflammatory macrophages (M1 macrophages) and macrophages involved in tissue homeo

71 ce had elevated cytotoxic T cells, increased M1 macrophages, and decreased M2 macrophages, indicating

72 or infiltration by activated CD8(+) T cells, M1 macrophages, and dendritic cells.

73 increased accumulation of CD8(+) T cells and M1 macrophages, and enhanced hepatosteatosis.

74 l differentiation of Ly6c(hi) monocytes into M1 macrophages, and increased macrophage content and les

75 d neutrophil accumulation, the prevalence of M1 macrophages, and the severity of tissue damage.

76 ling phase of AKI supports the resolution of M1 macrophage- and TNF-alpha-dependent renal inflammatio

77 In M1 macrophages, APN induced proinflammatory cytokines, T

78 , and Raw264.7 macrophages demonstrated that M1 macrophage apoptosis was promoted by conditioned medi

79 Such ChemR23-expressing M1 macrophages are chemotactic to chemerin, whereas M2 m

80 While M1 macrophages are considered beneficial in asthma and c

81 M1 macrophages are highly glycolytic, whereas M2 macroph

82 eed, we present novel data showing that only M1 macrophages are neurotoxic and M2 macrophages promote

83 M1 macrophages are pro-inflammatory and have microbicida

84 Classically activated (M1) macrophages are known to play a role in the developm

85 we show that iNos-positive proinflammatory (M1) macrophages are recruited into the kidney in the fir

86 Macrophages undergoing classical activation (M1 macrophages) are proinflammatory, whereas alternative

87 skeletal muscle, thus identifying SHP-1 and M1 macrophages as essential mediators of virus-induced m

88 cription factor IRF8 that induced downstream M1 macrophage-associated genes.

89 a)-dependent release of opioid peptides from M1 macrophages at injured nerves.

90 Ig reduces the percentage of proinflammatory M1 macrophages but increases the percentage of anti-infl

91 opolysaccharide- or interferon-gamma-induced M1 macrophages, but failed to do so in the interleukin 4

92 phages and that conditioned medium (CM) from M1 macrophages, but not from M0 and M2 macrophages, indu

93 ctions allowing human classically activated (M1) macrophages, but not resting (M0) or alternatively a

94 disease in IL-4Ralpha(-/-) mice that produce M1 macrophages by allowing T cell activation, by maintai

95 , selective induction of cell death in human M1 macrophages by SMs may be mediated by cIAP-2, RIPK-1,

96 In sepsis, M1 macrophages can compensate for hyperinflammation by a

97 rophage addition (P < 0.05), suggesting that M1 macrophages can downregulate osteoclastogenesis.

98 Proinflammatory M1 macrophages can phagocytose tumor cells, while anti-i

99 th the expression of genes characteristic of M1 macrophages, CD8(+) T cells, and NK cells, while inve

100 M1 macrophages (CD86(+)), rather than M2 macrophages (CD

101 bese VAT is predominated by pro-inflammatory M1 macrophages; cold exposure induces an M1-to-M2 shift

102 ght, and c) selectively targets inflammatory M1 macrophages concomitant with controlled release of th

103 In humans and mice, inflammatory M1 macrophages contribute to the progression of IBD wher

104 plex data revealed that densities of CD8 and M1 macrophages correlated with their respective cell phe

105 M1 macrophages could be elicited by administration of CD

106 ns with cytokines to differentiate them into M1 macrophages decreased their particle uptake.

107 CD11d-deficient M1 macrophages demonstrated improved migration in a thre

108 analysis to interrogate the transcriptome of M1 macrophages derived from mice with macrophage-specifi

109 d migration in response to sFasL compared to M1 macrophages derived from young animals.

110 M1 macrophages developed from interferon gamma (IFN-gamm

111 induced, but HRG-deficient serum prevented, M1 macrophage differentiation in vitro.

112 we found that IL-15, a cytokine that induces M1 macrophage differentiation, programs human peripheral

113 ce with IL-4 plus IL-13, or with M2a but not M1 macrophages, dramatically increased the generation of

114 etic kidney showed increased accumulation of M1 macrophages, elevated pro-inflammatory cytokines and

115 c activities and that classically activated (M1) macrophages exhibit greater phagocytic capacity than

116 es revealing a low score for HLA-DR positive M1 macrophages exhibited a better response to short-cour

117 fa), a key feature of classically activated (M1) macrophages, express fluorescent proteins Tg(mpeg1:m

118 The M1 macrophages expressed significantly higher levels of

119 thesized that HCMV induced a proinflammatory M1 macrophage following infection to promote viral disse

120 terize divergent gene expression patterns in M1 macrophages following standard polarization protocols

121 re spared, allowing them to polarize towards M1 macrophages for reactivation of immunity against brea

122 Under homeostatic conditions, M1 macrophage frequency was higher in the Ninj1(-/-) mou

123 DMRP(NOCas) specifically distinguishes M1 macrophages from other leukocytes including T cells,

124 nduce Th1 and Th17 cell differentiation than M1 macrophages from SOCS3(fl/fl) mice.

125 BL/6 mouse macrophages, we observed enhanced M1 macrophage function in vitro and in vivo.

126 In contrast, M1 macrophages gave higher levels of cysteinyl leukotrie

127 Herein, we show that human M1 macrophages generated by IFN-y and IL-12- and IL-18-s

128 The phagosomes of M1 macrophages had a similar buffering power and proton

129 In stark contrast to Th17 cells and M1 macrophages, high salt blunted the alternative activa

130 Thus, M1 macrophages, IFN-gamma-secreting Th1 cells, CD8+ T ce

131 In vivo, LiLa targets M1 macrophages in a mouse model of atherosclerosis, allo

132 Predominance of M1 macrophages in lethally-infected mice was associated

133 fferentiation of MDSCs into pro-inflammatory M1 macrophages in LuM, indicated that MDSC plasticity an

134 Excess oncostatin M (OSM) produced by M1 macrophages in the diabetic BM signals through p66Shc

135 ed accumulation of total and proinflammatory M1 macrophages in the obese AT, increased expression of

136 AZA-C + DFMO treatment and resulted in fewer M1 macrophages in the tumor microenvironment.

137 ed by increased presence of pro-inflammatory M1 macrophages in the tumour tissues.

138 ion, there were significantly more apoptotic M1 macrophages in tPA-deficient mice than their wild-typ

139 nges in the lymphocyte compartment and fewer M1 macrophages in visceral adipose tissue.

140 n macrophages in atherosclerotic lesions and M1 macrophages in vitro.

141 Expansion of M1 macrophages in vivo enhanced the recruitment and acti

142 the sponge prolonged the percentage of M and M1 macrophages, in addition to increasing the percentage

143 igh expression of IRF5 was characteristic of M1 macrophages, in which it directly activated transcrip

144 gamma DNA, which enhances the development of M1 macrophages, increased virus replication in the eye;

145 immune microenvironment by polarizing M2 to M1 macrophages, increasing CD4(+) and CD8(+) T cells, B

146 M1 macrophages incubated with NETs derived from patients

147 While proinflammatory M1 macrophages induce T1D, M2 macrophages have been show

148 gocytosis activity of M1 and M2 macrophages, M1 macrophage-induced autologous and allogeneic CD4(+) T

149 roved survival, likely due to higher TIL and M1 macrophage infiltration as well as lower intra-tumora

150 rthermore, there were higher lymphocytes and M1 macrophage infiltration in high mutation BCs.

151 inflammation associated with neutrophil and M1 macrophage infiltration into white adipose tissue.

152 Proinflammatory M1 macrophages initially are recruited to sites of injur

153 or (IFNgamma(hi)) CD8 T cells, and increased M1 macrophages (iNOS(hi), arginase(lo), and IL10(lo)); t

154 ethally-infected mice showed accumulation of M1 macrophages (iNOS-positive) in the liver.

155 O, inflammatory cytokines and trafficking of M1 macrophages into adipose tissue.

156 LCbeta2 plays an important role in switching M1 macrophages into an M2-like state.

157 y monocytes and accumulation of inflammatory M1 macrophages into developing atherosclerotic lesions.

158 uced infiltration of functional/inflammatory M1 macrophages into gingival tissue and alveolar bone re

159 eover, arglabin oriented the proinflammatory M1 macrophages into the anti-inflammatory M2 phenotype i

160 egulated in M2 macrophages and suppressed in M1 macrophages isolated from both mice and humans, and g

161 , the recent advances in drug delivery using M1 macrophages, macrophage-derived exosomes, and macroph

162 duced the expression of the pro-inflammatory M1 macrophage marker CD11c in HFD-fed wild-type mice.

163 atment, lung macrophages developed increased M1 macrophage marker expression during the first 2-3 wk,

164 expressed significantly higher levels of the M1 macrophage marker IL-1beta compared with macrophages

165 The expression of an M1 macrophage marker, inducible nitric oxide synthase (i

166 uction of nitric oxide synthase 2 (NOS2), an M1 macrophage marker, resulting in remodeling of the tum

167 Gene expression of Cd11c, the M1 macrophage marker, was decreased; while Cd206, the M2

168 le of Tregs in suppressing the expression of M1 macrophage markers (Tnfa, Il6, iNos, Ip10) and promot

169 ivated cell sorting indicate a prevalence of M1 macrophage markers and a reduction of M2 macrophage m

170 tion, TRX80 induced the expression of murine M1 macrophage markers through Akt2/mechanistic target of

171 macrophages and BMDM, expression of several M1 macrophage markers was elevated, whereas M2 markers w

172 rization, reduced expression of inflammatory M1 macrophage markers, supported resolution of inflammat

173 Persistence of inflammatory M1 macrophages may derail healing and compromise organ f

174 these results indicate that the presence of M1 macrophages may disrupt the generation of donor-type

175 However, the critical mechanism by which M1 macrophages mediate their anti-C. neoformans activity

176 l subsets suggested that activated NK cells, M1 macrophages, memory B cells, and follicular helper T

177 observed a sudden switch from the classical M1 macrophage (microbicidal) phenotype toward an alterna

178 there was an increase in the myeloid cells, M1 macrophages, monocytes, neutrophils, and other granul

179 hrough the proinflammatory response of their M1 macrophages (MPs).

180 esponse are associated with proinflammatory (M1) macrophages (MPs), resolution of inflammation is ass

181 ed in M2 macrophages and strongly reduced in M1 macrophages, observations that were recapitulated in

182 terleukin 4 treatment, but almost missing in M1 macrophages obtained by IFN-gamma and lipopolysacchar

183 olarization to the classical proinflammatory M1 macrophage or the alternative antiinflammatory M2 mac

184 gated the association between high level of "M1" macrophage or "M1"/"M2" ratio and the tumor immune m

185 sociated with Helper T-cells (p = 0.034) and M1 macrophages (p < 0.0001).

186 beta inhibits the "classically" activated or M1 macrophage phenotype during infection through negativ

187 Additionally, CpG-ODNs induce an M1 macrophage phenotype that restricts angiogenesis.

188 r, we demonstrated that LMW HA activated the M1 macrophage phenotype with the unique cPLA2alpha/COX2(

189 ss activation, but a lower prevalence of the M1 macrophage phenotype within atherosclerotic plaques.

190 ected mice also demonstrated induction of an M1 macrophage phenotype, indicated by upregulation of IL

191 that excess Galpha(i2) signaling promotes an M1 macrophage phenotype, whereas Galpha(i2) signaling de

192 inflammatory status that was indicative of a M1 macrophage phenotype.

193 titis environment, promoting the M2 over the M1 macrophage phenotype.

194 s in particular, accompanied by skewed M2 to M1 macrophage phenotype.

195 esponsible for the dominant proinflammatory (M1) macrophage phenotype in T2D wounds is unknown.

196 cells polarized infiltrating monocytes to an M1-macrophage phenotype, which released IL1beta and TNFa

197 M1 macrophages play a major role in worsening muscle inj

198 Treatment with GB1107 increased tumor M1 macrophage polarization and CD8(+) T-cell infiltratio

199 Our data suggest a critical role for IRF5 in M1 macrophage polarization and define a previously unkno

200 It suppresses M1 macrophage polarization and reciprocally promotes the

201 eNOS and nNOS mutant mice show comparable M1 macrophage polarization compared with wild-type contr

202 MAIT cells act in adipose tissue by inducing M1 macrophage polarization in an MR1-dependent manner an

203 We observed enhanced pulmonary M1 macrophage polarization in immunosuppressed (IS) host

204 promote M2 macrophage polarization, inhibit M1 macrophage polarization in periodontitis, and allevia

205 ic and polyamine-reducing therapy stimulates M1 macrophage polarization in the tumor microenvironment

206 suppressive leukocytes and facilitated M2-to-M1 macrophage polarization in the tumor.

207 g, RIG-I and MDA5 together are essential for M1 macrophage polarization in vivo and the control of WN

208 d, myeloid suppressor cells are reduced, and M1 macrophage polarization is increased in vivo.

209 rophages, and its ability to trigger a M2-to-M1 macrophage polarization switch might be therapeutical

210 propose that obesity and hypertension induce M1 macrophage polarization via mechanisms that directly

211 uggest that FENDRR enhances IFNgamma-induced M1 macrophage polarization via the STAT1 pathway.

212 e, an iNOS inhibitor, significantly enhances M1 macrophage polarization while S-nitroso-N-acetylpenic

213 Loss of MMP7 resulted in M1 macrophage polarization within H. pylori-infected sto

214 mice display enhanced classically activated M1 macrophage polarization without major effects on alte

215 In the late phase of M1 macrophage polarization, increased histone lactylatio

216 d: HIF-1alpha is induced by Th1 cytokines in M1 macrophage polarization, whereas HIF-2alpha is induce

217 TNF-alpha, IL-6, and IL-1beta and in limited M1 macrophage polarization.

218 rom iNOS in activated macrophages suppresses M1 macrophage polarization.

219 -acetylpenicillamine, a NO donor, suppresses M1 macrophage polarization.

220 d WT INS-GAS mice, and loss of MMP7 promoted M1 macrophage polarization.

221 pment of premalignant lesions by suppressing M1 macrophage polarization.

222 ation to the Fas death pathway and increased M1 macrophage polarization.

223 Kupffer cells, associated with a shift to an M1 macrophage polarization.

224 marrow-derived macrophages with EDPs induced M1 macrophage polarization.

225 some activation, neutrophil recruitment, and M1-macrophage polarization in response to P. aeruginosa

226 the fractions of mature dendritic cells and M1 macrophages, prevented the increase of regulatory T c

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

228 M1 macrophages primarily rely on glycolysis, whereas M2

229 FoxO1 expression in macrophages under M2 or M1 macrophage-priming conditions, respectively.

230 Classically activated (M1) macrophages produce proinflammatory mediators to com

231 our findings indicate that EndMT induced by M1 macrophages promotes infantile hemangioma regression

232 SOCS3-deficient M1 macrophages provide the microenvironment to polarize

233 A reduced M2/M1 macrophage ratio further improved treatment outcomes

234 with TIMP-1, whereas TIMP-1 silencing in M0/M1 macrophages rendered them both angiogenic.

235 vitro, while ImmTAC treatment leads to M2-to-M1 macrophage reprogramming both in vitro and in tebenta

236 -12 productions secreted primarily by M2 and M1 macrophages, respectively.

237 Here, we show that an M1 macrophage response is rapidly induced and then maint

238 crophages rescued the inflammatory antiviral M1 macrophage response, revealing reduction-oxidation-de

239 suggesting a dominant classically activated/M1 macrophage response.

240 s, ODC in macrophages tempers antimicrobial, M1 macrophage responses during bacterial infections thro

241 in the pancreas, and reduced proinflammatory M1 macrophage responses were observed.

242 uction in T1D by influencing proinflammatory M1 macrophage responses, and mechanistically linking oxi

243 mplementing these pathways in IRF5-deficient M1 macrophages restored bacterial clearance.

244 ltration of neutrophils and monocyte-derived M1 macrophages, resulting in significant tissue sparing

245 M2, rather than M1 macrophages, seem to be the inducers of SMAD7-mediate

246 dontitis model in which adoptive transfer of M1 macrophages showed a significantly lower level of bon

247 leading to the suppression of IRF5-targeted M1 macrophage signature gene activation.

248 cells as osteoclast precursors, addition of M1 macrophages significantly suppressed RANKL-induced os

249 on occurred exclusively in "proinflammatory" M1 macrophages, specific (68)Ga-DOTATATE ligand binding

250 tion was characterized by elevated levels of M1 macrophage-specific surface proteins, CD80 and CD38,

251 ved in M2 macrophages compared to the M0 and M1 macrophage subtypes and the monocyte model, THP-1.

252 macrophages were F4/80(+)CD11c(+) (antitumor M1 macrophages) suggesting it to be the reason behind de

253 estricted expression of ChemR23 in naive and M1 macrophages supports the role of ChemR23 in the attra

254 Thus, it is clear that tPA promoted M1 macrophage survival through its receptor LRP-1-mediat

255 Our results showed that activated M1 macrophages synthesize and secrete AGE-albumin, which

256 M1 macrophages target cancerous cells and, therefore, ca

257 that FENDRR was expressed 80-fold higher in M1 macrophages than that in M2 macrophages.

258 Unlike pro-inflammatory M1 macrophages that antagonize tumorigenesis, MMe macrop

259 ey lack IL-13-producting NKT cells, generate M1 macrophages that are cytotoxic for 4T1 via the produc

260 cible nitric oxide synthase (iNOS)-producing M1 macrophages that are tumoricidal for 4T1 tumor cells;

261 mice requires the activation of NO-producing M1 macrophages that are tumoricidal, the reduction in MS

262 Using M1 macrophages that have been exposed to bacteria as a m

263 ti-Axl mAb treatment significantly increased M1 macrophages that highly expressed inducible NO syntha

264 re the most potent cytokines produced by the M1 macrophages that induce in vitro EndMT.

265 n of pro-inflammatory, classically activated M1 macrophages that lyse muscle in vitro by NO-mediated

266 gram characteristic of classically activated M1 macrophages that participates in Th1 responses.

267 ver, despite strong upregulation of GLUT6 in M1 macrophages, the absence of GLUT6 did not alter M1 po

268 rther, we hypothesize that MMT is induced in M1 macrophages through a sequential combination of infla

269 macrophages reduce lysis of muscle cells by M1 macrophages through the competition of arginase in M2

270 o control adipose tissue inflammation, while M1 macrophages, TNF, and other inflammatory cytokines dr

271 he reduced susceptibility of Trpc3-deficient M1 macrophages to apoptosis.

272 rsion by hm12-LOX and promoted conversion of M1 macrophages to M2 phenotype, which produced more MaR1

273 Here we report that in human and mouse M1 macrophages TonEBP suppresses IL-10 expression and M2

274 hrough RvE1-mediated repolarization of human M1 macrophages toward resolution-type macrophages.

275 together, our data implicate TLR4-dependent, M1 macrophage trafficking/polarization into the CNS as a

276 Most strikingly, M1 macrophage-treated ECs isolated from patient hemangio

277 ation of CD4(+) T cells, CD8(+) T cells, and M1 macrophages; treatment with BITE induces pronounced t

278 ssion profiling showed that ECs treated with M1 macrophages, tumor necrosis factor-alpha, or IL-1beta

279 us 'lactate clock' in bacterially challenged M1 macrophages turns on gene expression to promote homeo

280 zing oxidative phosphorylation (OX PHOS) and M1 macrophages utilizing glycolysis.

281 ion of CSF1 receptor signaling and increased M1 macrophages via a mechanism independent of CD8(+) T c

282 A role for M1 macrophages was further supported by investigations s

283 and PM in vitro models, HSV-1 replication in M1 macrophages was markedly lower than in M2 macrophages

284 nflammation, whereas migration of CD11b(-/-) M1 macrophages was not affected.

285 multaneously, the number of pro-inflammatory M1-macrophage was enhanced.

286 In M1 macrophages, we identified a metabolic break at Idh,

287 The TsSP-induced effects in M1 macrophages were completely reversed by inhibiting hi

288 ejection of intraocular clone 2.1 tumors and M1 macrophages were involved in mediating tumor rejectio

289 w that patients with diabetes have increased M1 macrophages, whereas diabetic mice have increased CD1

290 ity, NK cell production of IFN-gamma induces M1 macrophages, which act as important effectors during

291 STAT6-deficient mice produce M1 macrophages, which contain high levels of NO and are

292 rnatively activated (M2) to proinflammatory (M1) macrophages, which limit tumor growth and metastasis

293 pressive M2 macrophages to immunostimulatory M1 macrophages, while alphaCD47 blocks CD47 tumor cell s

294 er, IL-1beta was demonstrated to increase in M1 macrophages, while IFN-gamma was not.

295 nitric oxide and interleukin-6 production in M1 macrophages, while promoting mitochondrial respiratio

296 Repolarization of ChemR23-expressing M1 macrophages with 10 nM RvE1 increases IL-10 transcrip

297 ulation of IL-12/IL-18-primed macrophages or M1 macrophages with agonists for TLR-2, TLR-3, or TLR-4

298 ate-13-acetate (PMA) and differentiated into M1 macrophages with IFNgamma or M2 macrophages with IL4.

299 e dominated by pro-inflammatory macrophages (M1 macrophages) with higher expression of osteopontin (O

300 LiLa particles were selectively deposited to M1 macrophages within inflamed adipose tissue, as demons