ライフサイエンスコーパス: tissue macrophage

1 ls and lymphocytes, but not to B-1a cells or tissue macrophages.

2 with calcium-dependent lectins expressed by tissue macrophages.

3 ithelial cells, and a subsequent increase in tissue macrophages.

4 e 1 (HIV-1) infects CD4(+) T lymphocytes and tissue macrophages.

5 ted reservoir of infectious HIV-1 virions in tissue macrophages.

6 and precursors of resident and inflammatory tissue macrophages.

7 dentify yolk sac EMPs as a common origin for tissue macrophages.

8 hemoattractant activity for F4/80(+)CD11c(-) tissue macrophages.

9 embryonic-derived but not postnatal-derived tissue macrophages.

10 pilosebaceous follicles and colocalized with tissue macrophages.

11 s in the frequency of M1- or M2-like adipose tissue macrophages.

12 s of peripheral blood monocytes and resident tissue macrophages.

13 bone marrow precursors, blood monocytes, and tissue macrophages.

14 finition, not terminally differentiated like tissue macrophages.

15 nctly and universally associated with mature tissue macrophages.

16 1(op/op) mice, which have reduced numbers of tissue macrophages.

17 electively expressed PPARgamma among resting tissue macrophages.

18 rences and expression pattern in the pool of tissue macrophages.

19 1/hnRNPA2B1 complex-bound miR-17/93 activate tissue macrophages.

20 severe depletion of resident osteoclasts and tissue macrophages.

21 solated mouse monocytes compared with mature tissue macrophages.

22 mune cells, including regulatory T cells and tissue macrophages.

23 KKepsilon) in liver, adipocytes, and adipose tissue macrophages.

24 1), such as plasmacytoid dendritic cells and tissue macrophages.

25 embryonic lineage that parallels vertebrate tissue macrophages.

26 but not monocytes, dendritic cells or other tissue macrophages.

27 ynthesized and secreted by liver, brain, and tissue macrophages.

28 igh-fat diet showed no reductions in adipose tissue macrophages.

29 and restraining the inflammatory products of tissue macrophages.

30 for cardiac valve remodeling as a source of tissue macrophages.

31 d monocytes, the latter differentiating into tissue macrophages.

32 progenitors give rise to blood monocytes and tissue macrophages.

33 ing, inflammatory macrophages or in resident tissue macrophages.

34 the establishment of persistent infection in tissue macrophages.

35 asis and thus represent a central feature of tissue macrophages.

36 was required to rapidly replenish destroyed tissue macrophages.

37 he nanoparticle ((VT680)Macrin) primarily in tissue macrophages.

38 e pathophysiology is manifested primarily in tissue macrophages.(1) In this issue of Blood, Campeau a

39 HIV-expressing cells were associated with tissue macrophages, a target of HIV infection.

40 ge territories and homeostatic regulation of tissue macrophage abundance through growth factor availa

41 Mechanisms involved in adipose tissue macrophage accrual continue to be elusive.

42 nce regarding dietary cholesterol on adipose tissue macrophage accrual, systemic inflammation and its

43 ay for erythrophagocytosis in the context of tissue macrophage accumulation and inflammation involvin

44 Stat3 in T cells in DIO mice affects adipose tissue macrophage accumulation and M2 phenotype.

45 and IL-13, in the induction of inflammatory tissue macrophage accumulation and/or hemophagocytosis.

46 eas overexpression of SirT1 prevents adipose tissue macrophage accumulation caused by chronic high-fa

47 t decreases blood glucose levels and adipose tissue macrophage accumulation in a high-fat, diet-fed m

48 ctors that potentially contribute to adipose tissue macrophage accumulation in obesity.

49 ice transgenic for IL-4 production developed tissue macrophage accumulation, disruption of splenic ar

50 i-IL-4 complexes, lead to substantial YM1(+) tissue macrophage accumulation, erythrophagocytosis with

51 lesterol added resulted in increased adipose tissue macrophage accumulation, local inflammation and c

52 s influence diet-induced obesity and adipose tissue macrophage accumulation, mice that were either wi

53 tion, indicating a possible role for adipose tissue macrophage activation.

54 atory response, resident and newly recruited tissue macrophages adhere to extracellular matrix and ce

55 Distinct populations of tissue macrophages also acquire context-specific functio

56 Depletion of visceral tissue macrophages also did not alter central nervous sy

57 nt anti-inflammatory effects with regards to tissue macrophage and neutrophil density following ureth

58 marked reduction in pro-inflammatory adipose tissue macrophages and activated CD8+ T cells.

59 lammatory cytokines in both isolated adipose tissue macrophages and adipocytes.

60 Microglia are the brain's tissue macrophages and are found in an activated state s

61 First, we show an altered distribution of tissue macrophages and blood monocytes in the absence of

62 y alveolar macrophages, in contrast to other tissue macrophages and blood monocytes.

63 earance of senescent neutrophils by resident tissue macrophages and DCs helps to set homeostatic leve

64 lia, whereas monocytes, dermal, and lymphoid tissue macrophages and DCs were unaffected.

65 tion with, and/or infection of CD4(+)CCR5(+) tissue macrophages and dendritic cells (DCs) play import

66 Recruited monocytes differentiate into tissue macrophages and dendritic cells, which sample ant

67 ious subsets, which are able to give rise to tissue macrophages and dendritic cells.

68 s used for identifying the complex origin of tissue macrophages and discuss the relative contribution

69 Its expression on tissue macrophages and epithelial cells suggests importa

70 venger receptor-induced apoptosis in primary tissue macrophages and in macrophage apoptosis in advanc

71 tment reduced peripheral blood monocytes and tissue macrophages and inhibited macrophage function in

72 an enzyme predominantly expressed in mature tissue macrophages and is implicated in several disease

73 In contrast, tissue macrophages and monocyte-derived macrophages in v

74 However, unlike tissue macrophages and similar to DCs, they homeostatica

75 row-derived progenitor cells into monocytes, tissue macrophages and some dendritic cell (DC) subtypes

76 f osteopontin in the accumulation of adipose tissue macrophages and the development of insulin resist

77 The selective expression of CR3 by tissue macrophages and the requirement of TLR2 inside-ou

78 type lectin, CD209, known to be expressed on tissue macrophages and to mediate the uptake of M. lepra

79 m for stromal cells (fibrocytes and possibly tissue macrophages) and CD8(+) T and CD21(+) B lymphocyt

80 eplication in fibrocytes (possibly including tissue macrophages) and T and B lymphocytes in the prese

81 itors, circulating blood monocytes, resident tissue macrophages, and dendritic cells (DCs) present in

82 ), CD4(+), CD8(+), and CD25(+)) lymphocytes, tissue macrophages, and dendritic cells (Iba-1(+) and CD

83 ystem comprising monocytes, dendritic cells, tissue macrophages, and granulocytes.

84 ransduction in dendritic cells, osteoclasts, tissue macrophages, and microglia.

85 sue inflammation, M1 polarization of adipose tissue macrophages, and the development of insulin resis

86 Resident tissue macrophages are activated by the fungal pathogen

87 Although tissue macrophages are anatomically distinct from one an

88 Tissue macrophages are critical contributors to HIV path

89 The origins of tissue macrophages are diverse, with evidence for local

90 Hepatic tissue macrophages are key players in orchestrating live

91 To determine whether tissue macrophages are productively infected, we used 3

92 s with surprising results; for example, most tissue macrophages are yolk sac derived, monocytes and m

93 In tissues, macrophages are exposed to metabolic, homeostat

94 If AMs, like most tissue macrophages, are sessile, then this numerical adv

95 we review evidence on the pathogenic role of tissue macrophages as long-term viral reservoirs in vivo

96 Tissue macrophages assume a distinct phenotype, designat

97 ocytes given to MCP-1 KO recipients, adipose tissue macrophage (ATM) accumulation is reduced by ~40%,

98 Obesity is associated with increased adipose tissue macrophage (ATM) infiltration, and rodent studies

99 microRNA (miR) in the regulation of adipose tissue macrophage (ATM) phenotype following treatment of

100 the expansion of adipose tissue and adipose tissue macrophage (ATM) polarization, in the current stu

101 While the role of adipose tissue macrophage (ATM) pro-inflammatory signalling in t

102 Adipose tissue macrophage (ATM) recruitment and activation play

103 etes has been known for decades, and adipose tissue macrophage (ATM)-associated inflammation has rece

104 metabolic programs that characterize adipose tissue macrophages (ATM) in obesity are poorly defined.

105 Here, we studied whether human adipose tissue macrophages (ATM) modulate cancer cell function.

106 lation of classically activated (M1) adipose tissue macrophages (ATMs) and the expression of proinfla

107 These adipose tissue macrophages (ATMs) are inflammatory and promote l

108 Adipose tissue macrophages (ATMs) are key players orchestrating

109 Adipose tissue macrophages (ATMs) change during metabolic stress

110 o-inflammatory cytokines secreted by adipose tissue macrophages (ATMs) contribute to chronic low-grad

111 We further showed that adipose tissue macrophages (ATMs) in lipodystrophy and obesity a

112 Here, we show that adipose tissue macrophages (ATMs) in obese mice secrete miRNA-co

113 s that NPY regulates the function of adipose tissue macrophages (ATMs) in response to dietary obesity

114 Adipose tissue macrophages (ATMs) infiltrate adipose tissue duri

115 We have examined the hypothesis that adipose tissue macrophages (ATMs) interact with and regulate the

116 Polarized activation of adipose tissue macrophages (ATMs) is crucial for maintaining adi

117 Adipose tissue macrophages (ATMs) play a critical role in obesit

118 Adipose tissue macrophages (ATMs) play an important role in the

119 ever, the functional role of IRF4 in adipose tissue macrophages (ATMs) remains unclear, despite high

120 ere we characterized the response of adipose tissue macrophages (ATMs) to weight loss and fasting in

121 d an increase in resident (CD11c(-)) adipose tissue macrophages (ATMs) when exposed to postnatal HFD.

122 and functional characteristics of adipocyte tissue macrophages (ATMs), in obese patients undergoing

123 en into account the heterogeneity of adipose tissue macrophages (ATMs), nor have they examined how ag

124 infiltration of increased numbers of adipose tissue macrophages (ATMs).

125 displayed cytotoxic activity toward adipose tissue macrophages (ATMs).

126 cent paradigm shifts in our understanding of tissue macrophage biology.

127 be specified, as they could be monocytes or tissue macrophages, but most likely dendritic cells.

128 n multiple organs during late gestation like tissue macrophages, but, unlike the latter, a majority o

129 omplexity is added by the new knowledge that tissue macrophages can be derived either from a resident

130 Tissue macrophages can be derived from embryonic progeni

131 Adipose tissue macrophages can contribute to the systemic proinf

132 l adipose tissue macrophage content (adipose tissue macrophages; CD11b(+), CD11c(+), Ly6C(hi)) concom

133 eatment with clodronate liposomes to deplete tissue macrophages, comparing the sites of (99m)Tc-EC20

134 Tissue macrophages comprise a heterogeneous group of cel

135 s are the first evidence that human urethral tissue macrophages constitute a principal HIV-1 reservoi

136 DPP-4i reduced visceral adipose tissue macrophage content (adipose tissue macrophages; C

137 or insulin action is associated with adipose tissue macrophage content (ATMc) and/or markers of macro

138 mice also had increased body fat and adipose tissue macrophage content, elevated plasma interleukin-6

139 e systemic inflammation or increased adipose tissue macrophage content, were reversed when plasma ins

140 a framework in which to consider how adipose tissue macrophages contribute to the remodeling events i

141 specific metabolic reprogramming of adipose tissue macrophages, contributing to the induction of tis

142 eripheral monocytes associated with death of tissue macrophages correlates with AIDS progression in m

143 ques, increasing monocyte turnover reflected tissue macrophage damage by SIV and was predictive of te

144 overt inflammation, constitutively maintain tissue macrophage/DC populations.

145 The recent recognition that tissue macrophages derive from different sources, couple

146 in the steady state, the dogma remains that tissue macrophages derive from monocytes.

147 While tissue macrophages derive from one of a small number of

148 ice selectively impacts CSF1R expression and tissue macrophage development in specific tissues.

149 nism by which parenchymal cells can modulate tissue macrophage differentiation and function.

150 man immunodeficiency virus (HIV) persists in tissue macrophages during antiretroviral therapy (ART),

151 and suggest that the relocation of iron from tissue macrophages during infection may contribute to an

152 poietic deletion of Ntn1 facilitates adipose tissue macrophage emigration, reduces inflammation and i

153 f diet-induced obesity, we show that adipose tissue macrophages exhibit reduced migratory capacity, w

154 Tissue macrophage export of iron occurs concurrent with

155 Reciprocally, adipose tissue macrophages express IL-17 and IL-22 receptors, ma

156 ba-1(+) and CD83(+)), with a small number of tissue macrophages expressing CD163 and CD204 scavenger

157 PM(2.5) increased adipose tissue macrophages (F4/80(+) cells) in visceral fat expr

158 Tissue macrophages, for example, are highly autofluoresc

159 Second, aside from being immune sentinels, tissue macrophages form integral components of their hos

160 The differentiation of resident tissue macrophages from embryonic precursors and that of

161 et Enrichment Analysis suggested that breast tissue macrophages from obese versus lean women are more

162 his study examines CXCL13 production by lung tissue macrophages from patients with IPF and the signal

163 We assessed gene expression in tissue macrophages from various mouse organs.

164 Tissue macrophages function to maintain homeostasis and

165 unctional Notch2 signaling promotes resident tissue macrophage gene expression signatures in monocyte

166 s co-implanted with freshly isolated adipose tissue macrophages grew more robustly than melanomas gro

167 ctional, and phenotypic heterogeneity within tissue macrophages has altered our understanding of thes

168 Tissue macrophages have an embryonic origin and can be r

169 Adipose tissue macrophages have been proposed as a link between

170 Since then, monocytes and tissue macrophages have emerged as key sentinels of infe

171 Macs is followed by their specification into tissue macrophages, hereby generating the macrophage div

172 Understanding the mechanisms that dictate tissue macrophage heterogeneity should explain why simpl

173 -wide analysis of gene expression in adipose tissue macrophages highlights the transforming growth fa

174 from the marrow through the blood to become tissue macrophages, histiocytes, and dendritic cells.

175 um enzyme levels through M-CSF regulation of tissue macrophage homeostasis without concomitant histop

176 factor-1 receptor (CSF-1R) kinase regulates tissue macrophage homeostasis, osteoclastogenesis, and P

177 of apoptotic cells is an innate function of tissue macrophages; however, its role in disease progres

178 e functional and phenotypic heterogeneity of tissue macrophages in different anatomic sites and as a

179 cells fail to recapitulate the phenotype of tissue macrophages in key respects, including that they

180 Our results reveal an unanticipated role for tissue macrophages in mesoangioblast function.

181 at altering the proinflammatory capacity of tissue macrophages in progressively HIV-infected individ

182 hemogenic endocardium is a de novo source of tissue macrophages in the endocardial cushion, the primo

183 al macrophages represent the largest pool of tissue macrophages in the human body and a critical inte

184 erleukin 4 and the alternative activation of tissue macrophages in the organismal response to diverse

185 vidence suggesting local self-maintenance of tissue macrophages in the steady state, the dogma remain

186 ytes do not show significant contribution to tissue macrophages in the steady state.

187 nounced proinflammatory signature of adipose tissue macrophages in type 2 diabetic obese patients, ma

188 tes engage different complement receptors on tissue macrophages in vivo.

189 nce, to our knowledge, of HIV persistence in tissue macrophages in vivo.

190 report that activation of different types of tissue macrophages, including microglia, by lipopolysacc

191 (IL-37tg) exhibit reduced numbers of adipose tissue macrophages, increased circulating levels of adip

192 Adipose tissue macrophage infiltration and inflammation were als

193 2DeltaLysM mice resisted HFD-induced adipose tissue macrophage infiltration and inflammatory cytokine

194 y cytokine, mediates obesity-induced adipose tissue macrophage infiltration and insulin resistance, i

195 Kinetics of adipose tissue macrophage infiltration was characterized by fluo

196 tion, adipocyte apoptosis, prevented adipose tissue macrophage infiltration, and protected against th

197 g of the failing myocardium reverses adipose tissue macrophage infiltration, inflammation, and adipon

198 correlated with the degree of IR and adipose tissue macrophage infiltration.

199 utaneous fat is inversely related to adipose tissue macrophage infiltration.

200 At the level of adipose tissue, macrophage infiltration and inflammation was dec

201 tissue factor-PAR2 signaling reduced adipose tissue macrophage inflammation, and specific pharmacolog

202 Lung tissue macrophage inflammatory protein-2, keratinocyte-d

203 downstream level, this lineage provides lung tissue macrophages (interstitial macrophages and tissue

204 sma lipids, increases autophagy, and orients tissue macrophages into an anti-inflammatory phenotype i

205 pronounced polarization of liver and adipose tissue macrophages into an M1 phenotype.

206 The reduction of synovial tissue macrophages is a reliable biomarker for clinical

207 y also suggest that its function in resident tissue macrophages is limited.

208 (MoM), we demonstrate that HIV infection of tissue macrophages is rapidly suppressed by ART, as refl

209 was found between the two genotypes, adipose tissue macrophages isolated from diet-induced obese Ucp2

210 clearance is primarily the function of fixed tissue macrophages (Kupffer cells) that line the hepatic

211 CL2(-/-) mice, despite no changes in adipose tissue macrophage levels, suggests that CCL2 has effects

212 ation of bone marrow precursors into adipose tissue macrophage-like cells.

213 f efferocytosis by resident murine and human tissue macrophages (Mo).

214 the origin and differentiation cues for many tissue macrophages, monocytes, and dendritic cell subset

215 Tissue macrophages (Mphis) and dendritic cells (DCs) pla

216 cally and functionally distinct from mammary tissue macrophages (MTMs).

217 rmed with DNA isolated from ischemic muscle, tissue macrophages (Mvarphis), and endothelial cells.

218 at monocytes are the immediate precursors of tissue macrophages needs to be refined based upon eviden

219 These findings support the theory that tissue macrophage numbers are regulated through local pr

220 ly fueled by heightened local proliferation, tissue macrophage numbers increased systemically.

221 Tissue macrophage numbers vary during health versus dise

222 ication-competent virus was rescued from the tissue macrophages obtained from these animals.

223 much less is known about microglia, resident tissue macrophages of the brain that originate from a di

224 Microglial cells are the resident tissue macrophages of the CNS and are widely recognized

225 As the tissue macrophages of the CNS, microglia are critically

226 Thus, tissue macrophages, once infected, have the characterist

227 light of recent advances in understanding of tissue macrophage ontogeny, their capacity for self-rene

228 e subset with notable nuances as compared to tissue macrophage ontogeny.

229 ently, it has become evident that most adult tissue macrophages originate during embryonic developmen

230 rain macrophages but are distinct from other tissue macrophages owing to their unique homeostatic phe

231 ence that obesity-related changes in adipose tissue macrophage phenotype could be mediated by adipocy

232 Our investigations reveal that the tissue macrophage phenotype is under discrete tissue-sel

233 s of cells, including mast cells, monocytes, tissue macrophages, platelets, eosinophils, endothelial

234 Because tissue macrophages play a critical role in removing apop

235 ealed that the endocardially derived cardiac tissue macrophages play a phagocytic and antigen present

236 Tissue macrophages play an important role in organ homeo

237 trated ER stress-induced rewiring of adipose tissue macrophage polarization by IRE1alpha activation,

238 e the nature, functions, and interactions of tissue macrophage populations within their microenvironm

239 properties that distinguish them from other tissue macrophage populations, we have optimized serum-f

240 In this study, we show that tissue macrophages present in the fetal mouse lung media

241 rion sequestration and destruction via local tissue macrophages, prion trafficking by B and dendritic

242 We have found that adipose tissue macrophages produce interleukin-10 (IL-10) upon f

243 Tissue macrophages provide innate defense against GAS, a

244 ant and positive correlation between adipose tissue macrophage quantification at MR imaging and P904

245 l variance in mice was correlated to adipose tissue macrophage quantification by using monoclonal ant

246 With tissue insult, resident tissue macrophages rapidly efflux to lymph nodes where t

247 Tissue macrophages rapidly recognize and engulf apoptoti

248 nclude that CCL2 is not critical for adipose tissue macrophage recruitment.

249 may contribute to obesity-associated adipose tissue macrophage recruitment.

250 As immune sentinels, tissue macrophages regulate immune activation and inflam

251 Here we show that adipose tissue macrophages regulate the age-related reduction in

252 oxide content (r = 0.87, P < .0001), adipose tissue macrophage-related inflammation at immunohistoche

253 itial events of monocyte migration to become tissue macrophages remain poorly understood.

254 ocytes, whereas dendritic cells and resident tissue macrophages remained unaltered.

255 s in tailoring the phenotype and function of tissue macrophages remains unknown.

256 approaches that could promote elimination of tissue macrophage reservoirs.

257 Our results reveal unique intra-tissue macrophage specialization and identify neuro-immu

258 Factors that govern tissue macrophage specialization are emerging.

259 We hypothesized that synovial tissue macrophages (STM), which persist in remission, co

260 We have identified a new tissue macrophage subset in the thymus and have discover

261 fy Ly6C as a marker of functionally discrete tissue macrophage subsets and support a model of selecti

262 but the transcriptional basis for producing tissue macrophage subsets remains unknown.

263 Human Cell Atlas, has already revealed novel tissue macrophage subsets.

264 ervations support a model according to which tissue macrophage subtype specification is distinct from

265 eptor of the Ig superfamily (CRIg), found on tissue macrophages such as synovial macrophages, has pro

266 of Siglec-1 in circulating SSc monocytes and tissue macrophages suggests that type I IFN-mediated act

267 Tissue macrophages synthesize neutrophil chemoattractant

268 These tissue macrophages tailor appropriate responses to exter

269 light marked heterogeneity in the origins of tissue macrophages that arise from hematopoietic versus

270 addition to CD4 T lymphocytes, HIV-1 infects tissue macrophages that can actively accumulate infectio

271 These results define a lineage of tissue macrophages that derive from the YS and are genet

272 a, causing strong effects on circulating and tissue macrophages that perdure long after cessation of

273 n resulted in a phenotypic change in adipose tissue macrophages that was characterized by upregulatio

274 review, we discuss the different origins of tissue macrophages, the transcription factors regulating

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

276 IL-4 was sufficient to drive accumulation of tissue macrophages through self-renewal.

277 show that obesity reprograms mammary adipose tissue macrophages to a pro-inflammatory metabolically a

278 Heparanase was required for adipose tissue macrophages to produce inflammatory mediators res

279 We postulate that the failure of tissue macrophages to remove senescent erythrocytes led

280 reduced, further confirming polarization of tissue macrophages toward an anti-inflammatory phenotype

281 n adipose tissue and polarization of adipose tissue macrophages toward an M2 alternatively activated

282 formed to evaluate the kinetics and monocyte/tissue macrophage turnover in Indian rhesus macaques (Ma

283 ilin-1 was diminished on blood monocytes and tissue macrophages under proinflammatory conditions.

284 veal that a distinct process exists in which tissue macrophages undergo rapid in situ proliferation i

285 attractive target for delivering antigens to tissue macrophages via Sn-mediated endocytosis.

286 Activation of NF-kappaB in tissue macrophages was assessed in mice that expressed a

287 b-PI3Kgamma(-/-) mice, the number of adipose tissue macrophages was similar to control, but displayed

288 s demonstrated that both circulating PMN and tissue macrophages were altered under inflammatory condi

289 Adipose tissue macrophages were detected and quantified with a 4

290 In contrast, epidermal Langerhans cells and tissue macrophages were largely preserved.

291 anemia of inflammation, iron accumulated in tissue macrophages, whereas a relative paucity of iron w

292 rominent players in this process are adipose tissue macrophages, which are a specialized leukocyte pr

293 d promotes alternative activation of adipose tissue macrophages, which are required for the increased

294 Moreover, skin-resident tissue macrophages, which encounter S. mansoni excretory

295 y promoted alternative activation of adipose tissue macrophages, which secrete catecholamines to indu

296 okines and decreased accumulation of adipose tissue macrophages, which were also preferentially biase

297 nitors and the independent myeloid system of tissue macrophages, whose regulation by local microenvir

298 y activates the production of NPY in adipose tissue macrophages with autocrine and paracrine effects.

299 Infiltrating cells included tissue macrophages, with an HLA-DR(+)CD14(+)CD45(+)CD68(

300 ations like neutrophils and F4/80(+) adipose tissue macrophages without any alterations in the freque