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 reased transcription from P3 in inflammatory M1 macrophages.

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

5 lammatory cells and also the polarization of M1 macrophages.

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

7 he maturation of immature myeloid cells into M1 macrophages.

8 both nonpolarized and classically polarized M1 macrophages.

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

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

11 can promote CKD symptoms via infiltration of M1 macrophages.

12 g pathway promoted MDSC differentiation into M1 macrophages.

13 irst few days and initially transformed into M1 macrophages.

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

15 eby inhibiting the generation of tumoricidal M1 macrophages.

16 ted infections which contained predominately M1 macrophages.

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

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

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

20 Moreover, M1 macrophages accumulated in the renal interstitial com

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

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

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

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

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

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

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

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

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

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

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

32 eprogramming of mitochondrial metabolism for M1 macrophage activation.

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

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

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

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

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

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

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

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

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

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

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

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

45 13 and requires the induction of tumoricidal M1 macrophages and lymphocytes combined with a reduction

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

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

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

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

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

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

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

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

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

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

56 In M1 macrophages, APN induced proinflammatory cytokines, T

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

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

59 While M1 macrophages are considered beneficial in asthma and c

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

61 M1 macrophages are pro-inflammatory and have microbicida

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

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

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

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

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

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

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

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

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

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

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

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

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

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

76 M1 macrophages could be elicited by administration of CD

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

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

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

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

81 M1 macrophages developed from interferon gamma (IFN-gamm

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

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

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

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

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

87 The M1 macrophages expressed significantly higher levels of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

106 Proinflammatory M1 macrophages initially are recruited to sites of injur

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

137 M1 macrophages play a major role in worsening muscle inj

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

139 It suppresses M1 macrophage polarization and reciprocally promotes the

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

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

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

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

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

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

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

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

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

149 pment of premalignant lesions by suppressing M1 macrophage polarization.

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

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

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

153 rom iNOS in activated macrophages suppresses M1 macrophage polarization.

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

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

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

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

158 SOCS3-deficient M1 macrophages provide the microenvironment to polarize

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

160 -12 productions secreted primarily by M2 and M1 macrophages, respectively.

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

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

163 suggesting a dominant classically activated/M1 macrophage response.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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