ライフサイエンスコーパス: M2 macrophage

1 by monocyte-derived macrophages (both M1 and M2 macrophages).

2 red due to low binding affinity of M2pep for M2 macrophage.

3 age chemoattraction and differentiation into M2 macrophage.

4 s of chemokine mRNA and increased numbers of M2 macrophages.

5 e for mTORC2 signalling in the generation of M2 macrophages.

6 reduction in apoptotic M1, but not apoptotic M2 macrophages.

7 Administration of IL-4 is known to augment M2 macrophages.

8 ytokines and chemokines in the M1 versus the M2 macrophages.

9 chment in markers of alternatively activated M2 macrophages.

10 0-fold higher in M1 macrophages than that in M2 macrophages.

11 hage content and an enrichment in markers of M2 macrophages.

12 mmatory M1 macrophages and anti-inflammatory M2 macrophages.

13 by selective induction of anti-inflammatory M2 macrophages.

14 can program naive monocytes to polarize into M2 macrophages.

15 d a concomitant enhancement in arginase-1(+) M2 macrophages.

16 immune evasion by establishing residency in M2 macrophages.

17 and oxidative metabolism, characteristic of M2 macrophages.

18 tes, polarizing them toward tumor-supporting M2 macrophages.

19 No such trends were observed for CD163+ M2 macrophages.

20 out major effects on alternatively activated M2 macrophages.

21 to do so in the interleukin 4 (IL4)-induced M2 macrophages.

22 r cells (MDSCs), and alternatively activated M2 macrophages.

23 eported for AM HC-HA-PTX3 on polarization of M2 macrophages.

24 tases with the exception of CD4+ T cells and M2 macrophages.

25 +)/IL-31(+) macrophages and CD68(+)/CD163(+) M2 macrophages.

26 myeloid-derived suppressor cells (MDSC), and M2 macrophages.

27 TNF-alpha levels were 5x higher with M1 vs. M2 macrophages.

28 in macrophage gene expression in both M1 and M2 macrophages.

29 d a significant reduction of pro-tumorigenic M2 macrophages.

30 1 inhibitor 3887 suppresses SPM formation in M2 macrophages.

31 nds of the spectrum are classified as M1 and M2 macrophages.

32 cytic capacity than alternatively activated (M2) macrophages.

33 gh the induction of alternatively activated (M2) macrophages.

34 ors reduce leukotrienes in M1 but less so in M2 macrophages, 3) zileuton blocks resolution-initiating

35 is, together with disturbed proportion of M1/M2 macrophages, accompanied by enhanced formation of art

36 NAMPT-primed M2 macrophages activate extracellular-regulated kinase 1

37 d direct-acting antiviral therapy attenuated M2 macrophage activation and associated liver fibrosis.

38 induced by OVA, affecting Th2 inflammation, M2 macrophage activation and skin barrier function.

39 (OVA), we investigated Th2 immune responses, M2 macrophage activation and skin barrier gene expressio

40 icular fungal species in the gut and promote M2 macrophage activation at distant sites to influence s

41 ccompanied by a shift toward pro-tumorigenic M2 macrophage activation in Slc7a2-deficient mice, as ma

42 polarized these cells to adopt either M1 or M2 macrophage activation phenotypes.

43 The combined effect of restrained M1 and M2 macrophage activation resulted in decreased productio

44 We showed that M2 macrophage activation was associated with liver fibro

45 The shift toward M2 macrophage activation was confirmed in bone marrow-de

46 Pro-tumorigenic M2 macrophage activation was diminished in myeloid-speci

47 The alterations in M1 and M2 macrophage activation were confirmed in bone marrow-d

48 ates a mechanism by which NaCl inhibits full M2 macrophage activation.

49 well-accepted but simplified paradigm of M1/M2 macrophage activation.

50 RP-39 deficiency was found to be involved in M2 macrophage activation.

51 sociated with alternative anti-inflammatory (M2) macrophage activation, including interleukin 4 (IL-4

52 components related to interferon activation, M2 macrophages, adaptive immunity, extracellular matrix

53 -/-), which exhibit a selective depletion of M2 macrophages after MI.

54 omitant increases in alternatively activated M2 macrophage and dendritic cell phenotypes.

55 ected mice lacking A2BAR exhibited decreased M2 macrophage and eosinophil recruitment and reduced IL-

56 ment, differential expression between M1 and M2 macrophages and a validation using genes causing mono

57 ificantly increased levels of protumorigenic M2 macrophages and beta-cateninSer552 (beta-CatSer552) e

58 rrelation was observed between the number of M2 macrophages and beta-cell replication.

59 SDF-1 expressing cells, HGF expressing Ym1+ M2 macrophages and CD133+ stem cells in the injury sites

60 d invasion, elevated CD8+ T cells, decreased M2 macrophages and decreased angiogenesis.

61 cancer growth with increased tumor-promoting M2 macrophages and decreased CD8(+) T cells.

62 in D1 did not promote the differentiation of M2 macrophages and did not promote tissue fibrosis.

63 impaired recovery, associated with decreased M2 macrophages and escalated microbial imbalance.

64 t model showed reduction of tumor-associated M2 macrophages and favored polarization towards an antit

65 in accumulation of inflammation-suppressing M2 macrophages and FOXP3(+) Tregs in plaques and reduced

66 Consequently, Gpr132 deletion reduces M2 macrophages and impedes breast cancer lung metastasis

67 sponse, mediated by a decrease of protumoral M2 macrophages and increased infiltration of antitumor C

68 (M2pep) that binds preferentially to murine M2 macrophages and M2-like TAMs.

69 ic tumor microenvironment that harbored more M2 macrophages and myeloid-derived suppressor cells.

70 mice that had a depleted ability to develop M2 macrophages and other in-vitro studies supported that

71 ct and selective depletion of protumorigenic M2 macrophages and promotes antitumor immunity, highligh

72 inhibitor-loaded nanoparticles (DNTs) target M2 macrophages and simultaneously inhibit CSF1R and SHP2

73 ation of eosinophils, but markedly decreased M2 macrophages and SPEM features, while eosinophil deple

74 icant reduction in both local IL33-producing M2 macrophages and SPEM in SAMP.

75 Dab2 expression was upregulated in M2 macrophages and suppressed in M1 macrophages isolated

76 ermore, we demonstrated that the decrease in M2 macrophages and TAMs, concomitant with the reduction

77 apable of downregulating the M2 phenotype in M2 macrophages and that the low expression of this miRNA

78 atment increased parasympathetic modulation, M2 macrophages and the anti-oxidant enzyme activity but

79 ethally infected mice showed polarization of M2 macrophages and their accumulation in peritoneum, but

80 hoblast cells, is able to induce homeostatic M2 macrophages and Tregs.

81 in M1 macrophages was markedly lower than in M2 macrophages and unstimulated controls.

82 d in reduced infiltration of protumorigenic (M2) macrophages and dramatically decreased ascites volum

83 mmune cells such as alternatively activated (M2) macrophages and Th17 cells play a role in the progre

84 ription factor PPARgamma is known to promote M2-macrophage and alveolar macrophage development.

85 to 1664 +/- 349 cells/mg; P < 0.01), M1 and M2 macrophages, and dendritic cells in perivascular adip

86 s of pro-tumorigenic alternatively polarized M2 macrophages, and lower levels of several chemokines a

87 umulation of regulatory T cells, mast cells, M2 macrophages, and markedly elevated transforming growt

88 ting effector T cells, increases a subset of M2 macrophages, and significantly prolongs survival in c

89 T cells as well as alternatively activated (M2) macrophages, and the induction of pulmonary histopat

90 In contrast, in M2 macrophages, APN induced the anti-inflammatory cytoki

91 Increased infiltration of M1, but not M2, macrophages appears to mediate the suppression of UU

92 The polarization processes for M1 versus M2 macrophages are quite distinct in the context of chan

93 Lung M2 macrophages are regulators of airway inflammation, as

94 Alternatively activated (also known as M2) macrophages are involved in the repair of various ty

95 stimulated naive monocytes to polarize into M2 macrophages as indicated by increased surface express

96 sion associated with alternatively activated M2 macrophages as well as expression of genes associated

97 in the PDL-tail and were mainly produced by M2 macrophages at the early stage and by activated myofi

98 the expression of Mrc1 and Chil1, markers of M2 macrophages at the MI zone.

99 ediates colonic homeostasis by modulating M1/M2 macrophage balance and preventing extensive dysbiosis

100 tions to improve our understanding of the M1-M2 macrophage balance and properly exploit it in tissue

101 mopoietic phenotype of increased circulating M2 macrophages but failed to affect plaque development.

102 A restricted the proliferation of protumoral M2 macrophages but increased the proliferation of antitu

103 containing liposomes killed activated murine M2 macrophages, but not Hut78 cells, demonstrating selec

104 12+ colon mesenchymal cells (CMCs) generated M2 macrophages by regulating their shape during recovery

105 M2 macrophages (CD11b+/CD206+) did not increase with RE,

106 M1 macrophages (CD86(+)), rather than M2 macrophages (CD206(+)), were the dominant macrophage

107 Finally, the M2 macrophage chemokine CCL17 was identified as an essen

108 ant perivascular infiltration of M1, but not M2, macrophages coincides with endothelial expression of

109 er tumor burden and infiltration of MDSC and M2 macrophages compared with LNs at other sites.

110 growth factor beta, a prominent cytokine of M2 macrophages, compared with control ISMC.

111 and contribute to the pathology of obesity, M2 macrophages contribute to the pathology of asthma, bu

112 Excessive activation of either M1 or M2 macrophages contributes to the pathology of many dise

113 M2 macrophages correlate with disease severity and poor

114 only increased levels of CCL18, a marker of M2 macrophages, correlate with low CD4+ T cell counts in

115 ammatory M1 to alternative anti-inflammatory M2 macrophages, could potentially display osteoclast-lik

116 red via enhanced levels of anti-inflammatory M2 macrophages coupled with an impaired sensitivity of s

117 Furthermore, it promoted the precursors of M2 macrophages, DCs and regulatory T cells.

118 ecific loss of TRPC3 showed that M1, but not M2 macrophages, deficient in Trpc3 are less susceptible

119 Importantly, a combined blocking M2 macrophage-derived factors TGF-beta, VEGF and SDF-1 a

120 han M2pepKLA to primary, bone marrow-derived M2 macrophage, desired selectivity was retained only wit

121 Frequency of M2 macrophages detection associated with short-term rela

122 HIF-2 expression and markers of M2 macrophage differentiation were decreased in response

123 and more glycolytic M1 phenotype, but not to M2 macrophage differentiation, which primarily relies on

124 immune responses and that it is required for M2 macrophage differentiation.

125 hat PRMT1 is necessary for c-Myc function in M2 macrophage differentiation.

126 tivated receptor gamma (PPARgamma)-dependent M2 macrophage differentiation.

127 insulin receptor substrate (IRS)-2, inducing M2 macrophage differentiation.

128 Collectively, these results suggest that M2 macrophages directly reduce the levels of HSV-1 laten

129 , whereas naive macrophages and IL-4-induced M2 macrophages do not express GLUT6 protein.

130 HA induces FoxP3 T regulatory cells in vivo, M2 macrophages drive transforming growth factor-beta and

131 tic granuloma pathology through induction of M2 macrophages during S. japonicum infection.

132 investigated, T regulatory cells and M0 and M2 macrophages emerged as the most strongly associated w

133 miR-155 was increased in M2-macrophages except in adalimumab-treated patients.

134 ulting in higher IL-13 expression levels and M2 macrophage expansion in adipose tissue.

135 ess was established by transferring purified M2 macrophages from PAM3 treated control donors into DSS

136 ction has also been described, as well as in M2 macrophage function under defined circumstances.

137 were increased in GF-fed offspring, as were M2 macrophage gene markers and tight junction-related ge

138 e proinflammatory M1 macrophages induce T1D, M2 macrophages have been shown to delay this autoimmune

139 EPS induces development of anti-inflammatory M2 macrophages in a TLR4-dependent manner, and these cel

140 -induced IRS-2 signaling and polarization of M2 macrophages in allergic inflammation.

141 Here, we discuss the roles for M1 and M2 macrophages in asthma and obesity, and propose a mode

142 ling, leading to dysfunctions of both M1 and M2 macrophages in chronic HCV infected patients.

143 Consequently, the proportion of M2 macrophages in inflamed colons was lower in AKAP12 KO

144 miR-140 deficiency promotes accumulation of M2 macrophages in irradiated lung tissues.

145 Our data suggests an upregulation of M2 macrophages in laser treated animals by the increasin

146 , consistent with a key role of arginase and M2 macrophages in myeloma elimination by Th2 cells.

147 ed the origin and functional requirement for M2 macrophages in regression in normolipidemic mice that

148 ge recruitment and increased polarization of M2 macrophages in the arterial wall.

149 The critical role of M2 macrophages in this process was established by transf

150 The M2 macrophages in turn were found to secrete high levels

151 ting the immune response toward either M1 or M2 macrophages in vivo, wild-type mice were injected wit

152 pro-inflammatory (M1) and anti-inflammatory (M2) macrophages in human breast adipose tissue, determin

153 The number of CD68(+)CD206(+) M2 macrophages increased three- to sixfold from >=6 days

154 lls, increased M1 macrophages, and decreased M2 macrophages, indicating that host Wnt5a promotes an i

155 Finally, M2 macrophages induced a DC-SIGN-dependent adhesion of h

156 CM) from M1 macrophages, but not from M0 and M2 macrophages, induced chemokine (C-X-C motif) ligand 1

157 eneic CD4(+) T cell activation, but promotes M2 macrophage-induced autologous and allogeneic CD4(+) T

158 These results suggest a critical role for M2 macrophage induction in chronic HCV-associated immune

159 ssion, and this was associated with impaired M2 macrophage infiltration of the primary tumors.

160 T helper type 2-skewed immune polarization, M2 macrophage infiltration, and endothelial-to-mesenchym

161 T helper type 2-skewed immune polarization, M2 macrophage infiltration, and endothelial-to-mesenchym

162 They also exhibited more adipogenesis with M2 macrophage infiltration, both of which were abolished

163 In vitro, M2 macrophages inhibit CD4(+) and CD8(+) T cells.

164 M2 macrophages, innate lymphoid type 2 cells (ILC2s), eo

165 ment of both eosinophils and IL33-expressing M2 macrophages into corpus tissues were evident in SAMP.

166 examined how the activation of alternative (M2) macrophages is affected by salt.

167 nt downstream infiltration of IL33-producing M2 macrophages leading to intestinalized SPEM in SAMP, s

168 C. innocuum stimulates tissue remodeling via M2 macrophages, leading to an adipose tissue barrier tha

169 on, and in liver sections, PRMT1, c-Myc, and M2 macrophage levels were strongly correlated with each

170 M2 macrophage-like TAMs were localized in the center of

171 CVc inhibits phagocytosis activity of M1 and M2 macrophages, M1 macrophage-induced autologous and all

172 Treatment with the CM from CYP4A10(high) M2 macrophages (M2) increased pre-metastatic niche forma

173 Cs suppressed cytokine production, increased M2 macrophage marker expression, and augmented phagocyti

174 diated upregulation of the anti-inflammatory M2 macrophage marker interleukin-4Ralpha (IL-4Ralpha).

175 hage marker, was decreased; while Cd206, the M2 macrophage marker, was increased in skeletal muscle o

176 ased expression of lysosomal acid lipase, an M2 macrophage marker.

177 iNos, Ip10) and promoting the expression of M2 macrophage markers (Mrc1, Arg1, Il10) in bone-marrow-

178 exhibited the lower levels of ER stress and M2 macrophage markers than those from cGVHD-affected mic

179 thin the brain and an elevated expression of M2 macrophage markers than those receiving cryptococcal-

180 CM of recovering colons and mainly expressed M2 macrophage markers.

181 hages polarize in local environments, M1 and M2 macrophages may coexist in different organs and may d

182 Gpr132 expression positively correlates with M2 macrophages, metastasis, and poor prognosis in patien

183 The seemingly opposing functions of M1 and M2 macrophages must be tightly regulated for an effectiv

184 shed an immunosuppressive milieu mediated by M2 macrophages, myeloid-derived suppressor cells, CD1d(h

185 ophages are chemotactic to chemerin, whereas M2 macrophages not expressing ChemR23 surface receptor a

186 M2 macrophages not only release TGFbeta1 to directly ind

187 y in the ICU is associated with an increased M2 macrophage number, increased vascular density, and an

188 Both PRMT1 levels and M2 macrophage numbers were significantly lower in livers

189 ived monocytes and "alternatively activated" M2 macrophages obtained by interleukin 4 treatment, but

190 investigated the possible effects of M1 and M2 macrophages on RANKL-induced osteoclastogenesis.

191 Th2 and M2 macrophage or microglia supernatants had neither a di

192 o nonstimulated conditions (M0), addition of M2 macrophages, or no macrophage addition (P < 0.05), su

193 was associated with greater infiltration of M2 macrophages (p = 0.011) and neutrophils (p = 0.055).

194 Furthermore, VEGFC administration reduced M2 macrophage pericystic infiltrate, which has been impl

195 macrophages by 4.6% (P = 0.07), whereas the M2 macrophage phenotype increased by 46.9% (P = 0.04).

196 mor-associated macrophages (TAMs) exhibit an M2 macrophage phenotype that suppresses anti-tumor immun

197 In healing wounds, the M1 toward M2 macrophage phenotype transition supports resolution o

198 omplex, which promotes the anti-inflammatory M2 macrophage phenotype, and assists TRXR1-regulated arr

199 ppression and miR-146a induction promote the M2 macrophage phenotype, resulting in amelioration of ac

200 e, and arginase-positive cells, indicating a M2 macrophage phenotype.

201 , a biomarker of the alternatively activated M2 macrophage phenotype.

202 in human proinflammatory M1 and proresolving M2 macrophage phenotypes that, upon exposure to Escheric

203 M1 and M2 macrophage phenotypes, which mediate proinflammatory

204 Alternatively activated M2 macrophages play an important role in maintenance of

205 M2 macrophages play an important role in tissue repair a

206 that reparative (alternatively activated or M2) macrophages play a role in repair of damaged tissues

207 inhibitors aspirin and celecoxib suppressed M2 macrophage polarization and decreased allergic airway

208 of colonic homeostasis caused by aberrant M1/M2 macrophage polarization and dysbiosis contributes to

209 IRE1alpha) as a critical switch governing M1-M2 macrophage polarization and energy balance.

210 Increased intermediate M1-M2 macrophage polarization and improved cognition in mil

211 Ces1/Ces1g ablation also promoted M2 macrophage polarization and induced hepatic cholester

212 by reducing plaque inflammation by promoting M2 macrophage polarization and Treg induction.

213 TSP-2 knockdown induced anti-inflammatory M2 macrophage polarization at 21 d; however, it did not

214 tion of gp130 signaling leads to a defective M2 macrophage polarization followed by exacerbated infla

215 f prostaglandin E(2) (PGE(2)), which induced M2 macrophage polarization in the lung.

216 tion, enhanced type 2 cytokine signaling and M2 macrophage polarization in the subcutaneous white fat

217 for gp130 signaling in myeloid cells during M2 macrophage polarization in vitro and in vivo.

218 dendritic cell maturation and did not induce M2 macrophage polarization in vitro.

219 we examined the expression profile of 16 M1/M2 macrophage polarization markers at 3 h and 7 d postin

220 rent genes in a pattern distinct from the M1/M2 macrophage polarization paradigm.

221 Obesity shifts the immune phenotype from M2 macrophage polarization to M1, which causes metabolic

222 , lower aortic valve leaflet area, increased M2 macrophage polarization, and improved echocardiograph

223 es the activation of key pathways leading to M2 macrophage polarization, including STAT3, STAT6, Krup

224 lular communication and pro-tumoral baseline M2 macrophage polarization, the Panc-1 cells were transf

225 d spare respiratory capacity, and induced an M2 macrophage polarization-associated gene profile.

226 ory molecule gene expression and (d) induces M2 macrophage polarization.

227 minal aortic aneurysm formation and increase M2 macrophage polarization.

228 acrophage differentiation, in turn affecting M2 macrophage polarization.

229 so modulate the immune response by promoting M2 macrophage polarization.

230 ulation of Fra-1 expression and induction of M2 macrophage polarization.

231 nd thermogenesis in SAT, in part by slanting M2 macrophage polarization.

232 ulatory factor 4, a transcription factor for M2 macrophage polarization.

233 Effective therapy targeting this M2 macrophage population is thus a promising adjuvant to

234 increases regulatory T cells which activate M2 macrophages, prevent T cell proliferation and reduce

235 In vitro data supported M2 macrophages promoting fibroblast differentiation and

236 progression of IBD whereas immunosuppressive M2 macrophages protect against colitis.

237 ted a high HC in vitro and an increase in M1/M2 macrophage ratio in vivo.

238 tors, enhanced vascularity, and decreased M1/M2 macrophage ratios may account for the enhanced tumori

239 D8(+) T-cell infiltration, (iii) enhanced M1/M2 macrophage ratios, (iv) inhibited tumor growth, (v) b

240 Conversely, anti-inflammatory M2 macrophages reduce inflammation and aid in wound heal

241 T cells, Ly6C(+) monocytes, and both M1 and M2 macrophages; reduced tubulointerstitial and glomerula

242 phages primarily rely on glycolysis, whereas M2 macrophages rely on the tricarboxylic acid cycle and

243 The M1 to M2 macrophage reprogramming that develops during LPS tol

244 1 macrophages are highly glycolytic, whereas M2 macrophages require a more oxidative nutrient metabol

245 67 levels in stromal cells, and a persistent M2 macrophage response through day 56.

246 ns revealed an increase in anti-inflammatory M2 macrophage responses in liver and spleen, as associat

247 As hypothesized, the number of M2 macrophages rose and disease severity decreased.

248 ation of any cytotoxic drug cargo, exhibited M2 macrophage-selective toxicity not observed in monoval

249 ariants were associated with UM risk; M1 and M2 macrophage-specific gene expression was associated wi

250 Human UM cells express M1 and M2 macrophage-specific genes, whose expression is associ

251 id A (SAA) are significantly up-regulated in M2 macrophages stimulated with IL-31, but not in IL-4 re

252 n, confocal staining for macrophages, M1 and M2 macrophage subtypes, alpha-actin, and DAPI was perfor

253 hages up-regulated markers characteristic of M2 macrophages such as CD163 and CD206.

254 ocytose tumor cells, while anti-inflammatory M2 macrophages such as tumor-associated macrophages (TAM

255 ytes to differentiate into immunosuppressive M2 macrophages, suggesting that PAM3 might be of benefit

256 e cold-induced recruitment of adipose tissue M2 macrophages, suggesting the role of CSF1R signaling i

257 T regulatory cells in vitro, and DHA-treated M2 macrophages suppress atopic dermatitis in mice.

258 We have previously identified an M2 macrophage-targeting peptide (M2pep) that binds prefe

259 s, PCTR1 levels were significantly higher in M2 macrophages than in M1 phenotype, along with members

260 xpressed inducible NO synthase and decreased M2 macrophages that expressed Arginase 1 and were found

261 , with concomitant enhancements in ILC2s and M2 macrophages that helped control adipose tissue inflam

262 rgistic activation of Arg1 by RA and IL-4 in M2 macrophages that involves feed forward regulation of

263 ymphoid cells, which promote polarization of M2 macrophages, thereby enhancing expansion of the Treg

264 0.6 cells/visual field; p < 0.05, n = 6) and M2 macrophages [though the infiltration of macrophages w

265 its monocyte differentiation to either M1 or M2 macrophages through TLR2, associated with impaired ST

266 This results in efficient repolarization of M2 macrophages to an active M1 phenotype, and superior p

267 ge arginase-1 is the only factor required by M2 macrophages to block T cells in G1, and this effect i

268 However, the contribution of M2 macrophages to cardiac repair after myocardial infarc

269 IMD repolarizes immunosuppressive M2 macrophages to immunostimulatory M1 macrophages, whil

270 ytokines and chemokines, converted bystander M2 macrophages to M1, upregulated antigen presentation m

271 not resting (M0) or alternatively activated (M2) macrophages, to prime resting autologous NK cells.

272 et for 12 weeks showed increased circulating M2 macrophages together with a reduction in plaque forma

273 61 and MGG8 models A2V reprogrammed protumor M2 macrophages toward the antitumor M1 phenotype.

274 se (TRAP)-positive cell induction than M0 or M2 macrophage transfer.

275 g in vivo and in vitro studies, we show that M2 macrophages trigger hepatocyte senescence and enhance

276 effects were associated with an increase of M2 macrophages (twice in relation to control animals) an

277 pulmonary type 2 immune response (Th2 cells, M2 macrophages, type 2 innate lymphoid cells, IL-33, IL-

278 n and bioenergetics of in vitro models, with M2 macrophages utilizing oxidative phosphorylation (OX P

279 ionship between duration of stay in the ICU, M2 macrophages, vascularization, and pancreatic cell rep

280 irect, selective depletion of protumorigenic M2 macrophages via attenuation of CSF1 receptor signalin

281 d higher CD302 expression in mouse M1 versus M2 macrophages was also noteworthy.

282 l field; p < 0.01, n = 6), the percentage of M2 macrophages was decreased (denervated vs intact: 31 +

283 Following EET, the change in M2 macrophages was positively associated with changes in

284 RalphaKO mice, a marked reduction of uterine M2-macrophages was detected, a cell type relevant for an

285 CSF-1 DNA, which enhances the development of M2 macrophages, was associated with reduced virus replic

286 (-/-) phenotype was in part due to increased M2 macrophages, we adoptively transferred wt macrophages

287 and selective binding of [M2pep]2-Biotin to M2 macrophages were achieved with at least 10-fold lower

288 Common lymphoid progenitor cells and M2 macrophages were found to increase in female samples

289 M0 and M2 macrophages were highly resistant to TKIs and maintai

290 M2 macrophages were increased with EGCG compared with pl

291 Increases in M2 macrophages were positively correlated with fiber hyp

292 of Th1/Th17 cells and the polarization of M1/M2 macrophages; whereas the systemic immune responses ap

293 umor edge causing proliferative expansion of M2 macrophages, which in turn promotes tumor growth.

294 ed to controls with a reciprocal decrease in M2 macrophages, which remained unchanged among pathologi

295 r molecule Rictor inhibits the generation of M2 macrophages while leaving the generation of classical

296 ntiated into M1 macrophages with IFNgamma or M2 macrophages with IL4.

297 y defined by the balance between M0, M1, and M2 macrophages, with distinct survival patterns by ER st

298 the 32 tested cytokines and chemokines than M2 macrophages, with HSV-1 infection significantly incre

299 focal histology demonstrated a prevalence of M2 macrophages within the aortic medium in mice treated

300 ng obese mice exhibited greater ratios of M1/M2 macrophages within the peritoneal and visceral adipos