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 vated macrophages (aaMs, also referred to as M2 macrophages).

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

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

5 can program naive monocytes to polarize into M2 macrophages.

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

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

8 immune evasion by establishing residency in M2 macrophages.

9 and oxidative metabolism, characteristic of M2 macrophages.

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

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

12 out major effects on alternatively activated M2 macrophages.

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

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

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

16 o-M1 polarization switch on human and murine M2 macrophages.

17 e phenotype to favor alternatively activated M2 macrophages.

18 hase (iNOS) for M1 and CD163 and FR-beta for M2 macrophages.

19 ferentiation of monocytes to tumor-promoting M2 macrophages.

20 CD4(+)CD25(+)FoxP3(+) regulatory T cells and M2 macrophages.

21 uction in aged macrophages and proangiogenic M2 macrophages.

22 tor (MR)-positive (CD68(+)MR(+)) alternative M2 macrophages.

23 nd increased proportion of anti-inflammatory M2 macrophages.

24 suppresses its own expression in M1 but not M2 macrophages.

25 ction by IL-4, the prototypical activator of M2 macrophages.

26 lular low-density lipoprotein by iron-loaded M2 macrophages.

27 lates LPS-mediated regulation of C3 in M1 or M2 macrophages.

28 4, IL-13, and M-CSF induce anti-inflammatory M2 macrophages.

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

30 chment in markers of alternatively activated M2 macrophages.

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

32 mmatory M1 macrophages and anti-inflammatory M2 macrophages.

33 by selective induction of anti-inflammatory M2 macrophages.

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

35 cytic capacity than alternatively activated (M2) macrophages.

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

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

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

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

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

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

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

43 M2 macrophage activation was impaired when MMP-28 was ab

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

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

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

47 y response and scar formation by suppressing M2 macrophage activation.

48 phages and microglia, suggestive of mixed M1/M2 macrophage activation.

49 otes neither classical (M1) nor alternative (M2) macrophage activation but elicits a pro-inflammatory

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

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

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

53 and IL-10 and stimulated the development of M2 macrophages, all of which contributed to the rapid re

54 ro IL-4 polarization of human monocytes into M2 macrophages also resulted in a gene expression profil

55 r to human cells, murine bone marrow-derived M2 macrophages also shut down their TIMP-1 expression an

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

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

58 ly in the healing cascade by stimulating the M2 macrophages and altering the granulation tissue compo

59 nstrate a preference for VACV replication in M2 macrophages and could assist in designing treatments

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

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

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

63 We also discuss emerging concepts for how M2 macrophages and helminth-modulated dendritic cells ca

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

65 Arginase I is a marker of murine M2 macrophages and is highly expressed in many inflammat

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

67 TIM) that suppress tumor immunity, including M2 macrophages and myeloid-derived suppressor cells (MDS

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

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

70 which results in enhanced differentiation of M2 macrophages and regulatory T cells, leading to the at

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

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

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

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

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

76 D163(+)/macrophage mannose receptor-positive M2 macrophages and tryptase-positive mast cells in NPs.

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

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

79 differentiation of alternatively activated (M2) macrophages and neutrophil efferocytosis.

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

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

82 L-10), endothelial cells/blood vessel lumen, M2 macrophages, and granulation tissue size without comp

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

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

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

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

87 icidal and tumoricidal activity, whereas the M2 macrophages are involved in tumor progression and tis

88 ut not with tryptase levels, suggesting that M2 macrophages are major CCL18-producing cells in NPs.

89 h markers of M2 macrophages, suggesting that M2 macrophages are major FXIIIA-producing cells in NP.

90 Lung M2 macrophages are regulators of airway inflammation, as

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

92 whereas alternatively activated macrophages (M2 macrophages) are generally anti-inflammatory.

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

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

95 erentially associates with anti-inflammatory/M2 macrophages at later stages of infection.

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

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

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

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

100 Levels of CCL18 correlated with markers of M2 macrophages but not with tryptase levels, suggesting

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

102 12+ colon mesenchymal cells (CMCs) generated M2 macrophages by regulating their shape during recovery

103 It is unclear whether the balance of M1 and M2 macrophages can be altered and whether this affects d

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

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

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

107 h special considerations for their effect on M2 macrophage-containing tumors.

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

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

110 M2 macrophages correlate with disease severity and poor

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

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

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

114 ing proof that angiogenic capacity of murine M2 macrophages depended on their TIMP-free proMMP-9, Mmp

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

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

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

118 Alternatively polarized M2 macrophages developed a markedly higher spare respira

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

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

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

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

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

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

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

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

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

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

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

130 antly increased the percentage of reparative M2 macrophages (F4/80(+)CD206(+)) in the infarcted myoca

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

132 Aged M2 macrophages had elevated Fas (CD95) expression and di

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

134 addition, M2pep is a useful tool for murine M2 macrophage identification and for modulating M2 macro

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

136 phages and decreased alternatively activated M2 macrophages in adipose tissue.

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

138 ells promote differentiation of monocytes to M2 macrophages in an IL-4 and CD1d-dependent process.

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

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

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

142 es, and the number of procollagen-expressing M2 macrophages in injured kidneys.

143 These data identify a role for M2 macrophages in iron handling, a process regulated by

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

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

146 taining was observed within CD68(+)/CD163(+) M2 macrophages in NP.

147 macrophage identification and for modulating M2 macrophages in other murine models of disease involvi

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

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

150 i) monocytes and increased the proportion of M2 macrophages in the CNS with associated improvement in

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

152 icantly increased alternative activation of (M2) macrophages in the livers compared to infected wild-

153 ns with cytokines to differentiate them into M2 macrophages increased the amount of particle uptake.

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

155 Only M2 macrophages induced angiogenesis at levels comparable

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

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

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

162 pression levels with microvessel density and M2 macrophage infiltration, confirming our in vitro resu

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

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

165 Furthermore, adoptive transfer of M2 macrophages into myeloid SOCS3-deficient mice leads t

166 ially induces the migration of proangiogenic M2 macrophages into the laser lesions and increases proa

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

168 In vitro, we confirmed that M2 macrophages lacking integrin-beta3 produced more TGF-

169 Alternative stimulation into M2 macrophages lead to increased foam cell formation by

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

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

172 Moreover, in iron-loaded M2 macrophages, LXR activation induces nuclear factor er

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

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

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

176 thase (iNOS) was higher and expression of an M2 macrophage marker, arginase-1 (Arg 1) was lower in tu

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

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

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

180 oid and positive for alternatively activated M2 macrophage markers.

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

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

183 therapy-mediated increase in tumor-promoting M2 macrophages may form an indirect mechanism for chemor

184 culum (ER) stress, a predominance of M1 over M2 macrophage membrane receptors, and decreased mRNA exp

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

186 Overproduction of FXIII-A by M2 macrophages might contribute to the excessive fibrin

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

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

189 M2 macrophages not only release TGFbeta1 to directly ind

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

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

192 However, M2 macrophages on iron exposure acquire a phenotype favo

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

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

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

196 classical versus alternatively activated (M1/M2) macrophage paradigm.

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

198 nnose receptor C, type 1 mRNA expression, an M2 macrophage phenotype marker.

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

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

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

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

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

204 ation and by promoting the anti-inflammatory M2 macrophage phenotype.

205 M1 and M2 macrophage phenotypes, which mediate proinflammatory

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

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

210 FD feeding, NKT cells are activated, promote M2 macrophage polarization and induce arginase 1 express

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 In NKT-deficient CD1d(-/-) mice, M2 macrophage polarization in adipose tissue is reduced

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 nhibitor Stattic decreased efferocytosis and M2 macrophage polarization in vitro, with a correlating

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 profile and promoted alternatively activated M2 macrophage polarization through secretory factors inc

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

223 roinflammatory cytokines, down-regulation of M2 macrophage polarization, and apoptosis of MNCs in the

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

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

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

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

232 ctedly associated with elevated alternative (M2) macrophage polarization in adipose tissue mediated b

233 +) cells, and display increased alternative (M2) macrophage polarization.

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

235 M2 macrophages, prevalent in lean adipose tissue, are in

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

237 M2 macrophages produced SPM including maresin-1 (299 +/-

238 ng MyoD or myogenin expression, showing that M2 macrophages promote the early, proliferative stage of

239 In vitro data supported M2 macrophages promoting fibroblast differentiation and

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

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

242 Conversely, uptake of apoptotic PMN by M2 macrophages reduced ( approximately 25%) overall LM.

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

244 These data suggest that M2 macrophages represent a unique niche for long-term in

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

246 with IFN-gamma and IL-4, agonists of M1 and M2 macrophages, respectively, and their gene expression

247 s proinflammatory (M1) or anti-inflammatory (M2) macrophages, respectively.

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

249 Adoptively transferred mast cells or M2 macrophages reversed the heightened pancreatitis in t

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

251 ntained an enhanced alternatively activated (M2) macrophage signature in the lungs, which we have pre

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

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

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

255 on with redistribution toward protumorigenic M2 macrophage subsets, increased proliferation, hyperact

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

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

258 Levels of FXIII-A correlated with markers of M2 macrophages, suggesting that M2 macrophages are major

259 kers for anti-inflammatory/homeostatic human M2 macrophages suggests their potential therapeutic valu

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

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

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

263 -7c is expressed at a higher level in M-BMM (M2 macrophages) than in GM-BMM (M1 macrophages).

264 cells, was found to promote the formation of M2 macrophages that are thought to contribute to metasta

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

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

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

268 C/EBPbeta, a hallmark of M2 macrophages that regulates Arg1, was up-regulated upo

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

270 0.6 cells/visual field; p < 0.05, n = 6) and M2 macrophages [though the infiltration of macrophages w

271 ositive tumor cells can interact with M1 and M2 macrophages through CD200-CD200R-compex, and downregu

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

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

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

275 leased FetA into the medium, which polarized M2 macrophages to M1.

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

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

278 pression of ER stress shifted differentiated M2 macrophages toward an M1 phenotype and subsequently s

279 61 and MGG8 models A2V reprogrammed protumor M2 macrophages toward the antitumor M1 phenotype.

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

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

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

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

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 M0 and M2 macrophages were highly resistant to TKIs and maintai

289 Resident CD163(+) M2 macrophages were increased in HC-protected rats.

290 ended on their TIMP-free proMMP-9, Mmp9-null M2 macrophages were nonangiogenic, although their TIMP-1

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

292 f tumor cell lines to induce IL-10-producing M2 macrophages, which displayed increased levels of acti

293 M2 macrophages, which have been described as promoting t

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

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

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

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