ライフサイエンスコーパス: CSF-1

1 CSF-1 acted in part by inducing Mphi proliferation and i

2 CSF-1 activates a multitude of signaling pathways result

3 CSF-1 and CSF-1R were coexpressed in RCCs and TECs proxi

4 CSF-1 and IL-34 are present in saliva and seem to have c

5 CSF-1 deficiency decreased macrophage infiltration by ap

6 CSF-1 engagement of CSF-1R promoted RCC survival and pro

7 CSF-1 expression in TECs did not compensate for IL-34 de

8 CSF-1 has three biologically active isoforms: a membrane

9 CSF-1 heightened monocyte proliferation in the bone marr

10 CSF-1 injections increased counts in wild-type and mutan

11 CSF-1 is a major myeloid cell mitogen, and signaling thr

12 CSF-1 is central to kidney repair and destruction.

13 CSF-1 mediates Mo-dependent destruction in lupus-suscept

14 CSF-1 neutralization, but not of GM-CSF, in normal mice

15 CSF-1 receptor (CSF1R) signaling is important for the re

16 CSF-1(-/-) mice were not protected from ileus.

17 CSF-1, MIF, and MIG levels in both serum and saliva did

18 CSF-1, required for macrophage (Mo) survival, proliferat

19 d by macrophage colony-stimulating factor 1 (CSF-1) and receptor activator of nuclear factor-kappaB l

20 N-gamma) DNA or colony-stimulating factor 1 (CSF-1) DNA prior to ocular infection with HSV-1.

21 he receptor for colony-stimulating factor 1 (CSF-1) in steady-state conditions.

22 Colony-stimulating factor 1 (CSF-1) receptor (CSF-1R, or macrophage CSF receptor [M-C

23 Colony stimulating factor 1 (CSF-1) recruits tumor-infiltrating myeloid cells (TIM) t

24 ing, KIT, FLT3, colony-stimulating factor 1 (CSF-1), and RET, which are involved in a number of malig

25 Colony-stimulating factor 1 (CSF-1), the cytokine acting as the principal regulator o

26 in concert with colony-stimulating factor 1 (CSF-1)-dependent donor macrophages, induce a transformin

27 ion by limiting colony-stimulating factor 1 (CSF-1)-dependent proliferation and beta-catenin/cyclinD1

28 ust increase in colony-stimulating factor 1 (CSF-1)-directed motility was observed in macrophages def

29 N) (CX3CL1) and colony-stimulating factor 1 (CSF-1).

30 The cytokine colony stimulating factor-1 (CSF-1) acts as an important regulator of these macrophag

31 Colony-stimulating factor-1 (CSF-1) and its receptor (CSF-1R) have been implicated in

32 in response to colony-stimulating factor-1 (CSF-1) and receptor activator of NF-kappaB ligand (RANKL

33 mice that lack colony stimulating factor-1 (CSF-1) but are absent in CSF-1 receptor-deficient mice.

34 factor (EGF) or colony-stimulating factor-1 (CSF-1) can induce invasion through an EGF/CSF-1 paracrin

35 also suppressed colony-stimulating factor-1 (CSF-1) expression and reduced macrophage recruitment to

36 hages depend on colony stimulating factor-1 (CSF-1) for differentiation and survival.

37 mutation in the colony-stimulating factor-1 (CSF-1) gene (Csf1(tl)).

38 mutation in the colony-stimulating factor-1 (CSF-1) gene, we show that CSF-1-dependent macrophage fun

39 Colony-stimulating factor-1 (CSF-1) is expressed by kidney tubules at the onset of LN

40 Colony stimulating factor-1 (CSF-1) is the primary growth factor for macrophages, and

41 Blockade of colony-stimulating factor-1 (CSF-1) limits macrophage infiltration and improves respo

42 treatment with colony-stimulating factor-1 (CSF-1) was detected globally as early as 30 s and remain

43 Colony-stimulating factor-1 (CSF-1), the principal growth factor for macrophages, is

44 islet cancer to colony-stimulating factor-1 (CSF-1)-deficient Csf1(op/op) mice, which have reduced nu

45 Colony-stimulating factor-1 (CSF-1)-induced CSF-1 receptor (CSF-1R) tyrosine phosphor

46 Colony-stimulating factor-1 (CSF-1)-stimulated CSF-1 receptor (CSF-1R) tyrosine phosp

47 d growth factor colony-stimulating factor-1 (CSF-1).

48 the macrophage colony-stimulating factor-1 (CSF-1).

49 ppaB ligand and colony-stimulating factor-1 (CSF-1).

50 control of both colony stimulating factor-1 (CSF-1, or M-CSF) and receptor activator of NF-kappaB lig

51 Expression of IL-34, CSF-1 and the CSF-1R were maximal during early postnatal

52 by conversion of IL-4Ralpha(+) MPhis from a CSF-1-dependent to -independent program of proliferation

53 Cutaneous cGVHD developed in a CSF-1/CSF-1R-dependent manner, as treatment of recipient

54 Moreover, administration of a CSF-1 receptor-specific (CSF-1R-specific) antibody after

55 t E2fs are important downstream targets of a CSF-1 signaling cascade involved in myeloid development.

56 Here, we show that a CSF-1-dependent autocrine pathway is also responsible fo

57 e hypothesis that UVB triggers CLE through a CSF-1-dependent, macrophage (Mo)-mediated mechanism in M

58 d and its receptor in tumor cells leads to a CSF-1/CSF-1R autocrine loop which contributes to the agg

59 Thus, sunlight triggers a CSF-1-dependent, Mo-mediated destructive inflammation in

60 ows that PLCgamma1 controls OC numbers via a CSF-1-dependent DAG/beta-catenin/cyclinD1 pathway.

61 irect in vivo studies to determine whether a CSF-1 autocrine signaling loop functions in human breast

62 ts-2-mediated HER2 expression and activating CSF-1 expression for macrophage recruitment.

63 eatment of NOD mice with an antibody against CSF-1 receptor reduced diabetes incidence and led to the

64 lantation, and lung cGVHD was also IL-17 and CSF-1/CSF-1R dependent.

65 IL-34 and CSF-1 share a receptor (c-FMS), and both cytokines media

66 of this receptor and its ligands, IL-34 and CSF-1, in the brain are poorly understood.

67 nal up-regulation of PU.1, Irf-4, Irf-8, and CSF-1, genes critical for DC differentiation, and are ab

68 TLR4 chimeras and CSF-1-dependent macrophage-deficient mice were subjected

69 ogenic factor, MIP-1alpha, were elevated and CSF-1 receptor (CSF-1R)-dependent production of MIP-1alp

70 we have examined the expression of c-fms and CSF-1 in cervical tumor (n = 17) and normal cervix (n =

71 e primary growth factor for macrophages, and CSF-1 deficiency protects MRL-Fas(lpr) mice from kidney

72 The combination of RANKL and CSF-1 concurrently increased the levels of MAPK-phosphor

73 s have been implicated in tissue repair, and CSF-1, the principal macrophage growth factor, is expres

74 hibition, regulatory T-cell restoration, and CSF-1 inhibition.

75 riodontal disease: IL-34 in steady-state and CSF-1 in inflammation.

76 pletion of MR(hi) dermal macrophages by anti-CSF-1 receptor antibody reversed the nonhealing phenotyp

77 Strategies that deplete (anti-CSF-1 antibodies and CSF-1R inhibition) or stimulate (ag

78 Diabetes occurred in the anti-CSF-1 receptor protected mice after treatment with a blo

79 ence of diabetes, NOD mice treated with anti-CSF-1 receptor starting at 3 or 10 wk of age still conta

80 There was a positive correlation between CSF-1 and MMP-8, which both correlated negatively to IL-

81 T1A and CMT1X, as well as in human biopsies, CSF-1 is predominantly expressed by endoneurial fibrobla

82 onal studies showed that rhBARF1 could block CSF-1 cytokine signaling as well as EBV BARF1, whereas t

83 iculon-1 in macrophage migration toward both CSF-1 and CCL2 was confirmed.

84 tissue densities, are locally controlled by CSF-1, a pleiotropic growth factor whose in situ level o

85 ian (Xenopus laevis) Mphis differentiated by CSF-1 and IL-34 are highly susceptible and resistant to

86 Macrophage populations elicited by CSF-1 are associated with, and exacerbate, a broad spect

87 proliferation that was slightly enhanced by CSF-1, indicating that Tyr-559 has a positive Tyr-807-in

88 ) which is now known to be bound not only by CSF-1, but also by the unrelated interleukin-34 (IL-34)

89 n of detrimental macrophages is regulated by CSF-1, a cytokine that is mostly expressed by fibroblast

90 Levels of calprotectin, CSF-1, MIF, MIG, and MMP-8 were measured using enzyme-li

91 oform responsible for increasing circulating CSF-1 and, along with the csCSF-1 isoform, for increasin

92 This is based on high levels of circulating CSF-1 in patient sera with aggressive disease and increa

93 Taken together, circulating CSF-1 is a potential therapeutic target for lupus nephri

94 ivity results from three primary components, CSF-1/IL-34, TGF-beta2, and cholesterol.

95 in (JMD) Y559F mutations severely compromise CSF-1-regulated proliferation and differentiation.

96 dation of the cellular pathways that control CSF-1 expression may provide novel strategies for the re

97 onuclear phagocytes (MNPs), but the critical CSF-1 signals for these functions are unclear.

98 w-derived macrophages (BMDM) grown in M-CSF (CSF-1) have been used widely in studies of macrophage bi

99 GM-CSF and M-CSF (CSF-1) induce different phenotypic changes in macrophage

100 Conversely, administration of the cytokine CSF-1 before transplant expanded the host macrophage poo

101 d use of an ex vivo gene transfer to deliver CSF-1 intradermally, we determined that CSF-1 induces CL

102 e driven by an epidermal growth factor (EGF)/CSF-1 paracrine loop between tumor cells and host macrop

103 1 (CSF-1) can induce invasion through an EGF/CSF-1 paracrine loop between cancer cells and macrophage

104 ion of transgenic MMTV-PyMT tumors in an EGF/CSF-1-dependent manner.

105 HRG-beta1 or CXCL12 is dependent on the EGF/CSF-1 paracrine loop, invasion induced by EGF is not dep

106 iveness to HRG-beta1 is dependent on the EGF/CSF-1 paracrine loop.

107 ced by other ligands also relies on this EGF/CSF-1 paracrine invasive loop.

108 tients with lupus nephritis, and eliminating CSF-1 suppresses lupus in MRL-Fas(lpr) mice.

109 ylglyoxal reduced the release of endothelial CSF-1 (M-CSF), which stimulates polarization of macropha

110 vity in cervical cancer cells, which express CSF-1 and c-fms, resulted in increased apoptosis and dec

111 Macrophage colony-stimulating factor (CSF-1) is a key regulatory cytokine for amelogenesis, an

112 ion of macrophage colony-stimulating factor (CSF-1) signaling blocked macrophage/dendritic cell proli

113 Macrophage-colony stimulating factor (CSF-1) signaling through its receptor (CSF-1R) promotes

114 n that macrophage colony-stimulating factor (CSF-1; M-CSF) directly instructed myeloid commitment in

115 signaling through an epidermal growth factor-CSF-1 paracrine loop.

116 responses to the colony-stimulating factors CSF-1 and CSF-2 in vitro.

117 hat macrophages only partially accounted for CSF-1-dependent tubular repair.

118 ory conditions and reveal a central role for CSF-1 in the coordination of Mphi and DC homeostasis.

119 ylaxis throughout all chemotherapy cycles (G-CSF 1-6 cycles) with prophylaxis during the first two cy

120 phylaxis during the first two cycles only (G-CSF 1-2 cycles).

121 G-CSF 1 to 6 cycles arm compared with the G-CSF 1 to 2 cycles arm was euro 13,112 per patient with e

122 ected, FN-related costs were higher in the G-CSF 1 to 2 cycles arm.

123 y arm (eight of 84 patients) to 36% in the G-CSF 1 to 2 cycles study arm (30 of 83 patients), whereas

124 cremental cost effectiveness ratio for the G-CSF 1 to 6 cycles arm compared with the G-CSF 1 to 2 cyc

125 incidence of FN increased from 10% in the G-CSF 1 to 6 cycles study arm (eight of 84 patients) to 36

126 A higher CSF-1/IL-34 ratio was observed in patients with periodon

127 Patients with periodontitis displayed higher CSF-1 and MMP-8 levels in saliva compared with healthy p

128 However, CSF-1-deficient mice were able to produce significant le

129 ogy resulted in faithful expression of human CSF-1 in these mice both qualitatively and quantitativel

130 Here, we report that human CSF-1 knockin mice show augmented frequencies and functi

131 In addition, humanized CSF-1 mice will be a valuable experimental model to stud

132 and progenitor cells (CD34(+)) in humanized CSF-1 (CSF1(h/h)) newborn mice resulted in more efficien

133 ytes/macrophages obtained from the humanized CSF-1 mice show augmented functional properties includin

134 acrophages in inhibiting GVHD and identifies CSF-1 as a potential prophylactic therapy to limit acute

135 We investigated the role of BMP-2 in CSF-1 expression in osteogenic C2C12 cells.

136 imulating factor-1 (CSF-1) but are absent in CSF-1 receptor-deficient mice.

137 In the tumors that did develop in CSF-1-deficient animals, however, there were no signific

138 loskeletal disease; however, the increase in CSF-1 levels was far greater in LN.

139 restore or overexpress distinct isoforms in CSF-1-deficient (osteopetrotic) Cx32def mice, we demonst

140 he skin, and CLE in MRL-Fas(lpr), but not in CSF-1-deficient MRL-Fas(lpr) mice.

141 ingly, several cytokines were upregulated in CSF-1-deficient RT2 tumors, and neutrophil infiltration

142 onsive to the same growth factors (including CSF-1), express the same surface markers (including CD11

143 r, hypoxic TECs release mediators, including CSF-1, that are responsible for stimulating the expansio

144 lone or in combination with Smad 4 increased CSF-1 transcription.

145 GF-BB is a mitogen for MEOE-3M and increases CSF-1 protein levels, predominantly by transcription.

146 Increasing CSF-1 hastens renal healing after I/R in lupus-resistant

147 re are shared and unique roles of individual CSF-1 isoforms during renal inflammation.

148 Colony-stimulating factor-1 (CSF-1)-induced CSF-1 receptor (CSF-1R) tyrosine phosphorylation and ubi

149 In conclusion, I/R induces CSF-1 in injured TECs that expands aberrant Mo (M1 pheno

150 itonitis, and LPS-induced lung inflammation, CSF-1 neutralization lowered inflammatory macrophage num

151 and PU.1 as nuclear effectors that integrate CSF-1/RANKL signals during osteoclast differentiation to

152 rrelated with lupus activity, and intrarenal CSF-1 expression correlated with the histopathology acti

153 hat blocking both circulating and intrarenal CSF-1 may be necessary for therapeutic efficacy.

154 levels correlated with increasing intrarenal CSF-1 expression and histopathology.

155 e csCSF-1 isoform, for increasing intrarenal CSF-1.

156 her systemic CSF-1, as opposed to intrarenal CSF-1, promotes macrophage-dependent lupus nephritis rem

157 he serum or urine correlates with intrarenal CSF-1 expression and histopathology (increased macrophag

158 icated that in comparison with the X. laevis CSF-1-Mphis, the IL-34-Mphis express substantially great

159 iven the involvement of c-fms and its ligand CSF-1 in gynecologic cancers, such as that of the uterus

160 While the CSF-1R-cognate ligands, CSF-1 and interleukin-34 (IL-34) compete for binding to

161 Further mechanistic investigations linked CSF-1 and epidermal growth factor signaling in RCCs.

162 liferation was controlled by a rise in local CSF-1 levels, but IL-4Ralpha expression conferred a comp

163 In conclusion, IL-34-dependent, Mo-mediated, CSF-1 nonredundant mechanisms promote persistent ischemi

164 AG levels, we demonstrate that DAG modulates CSF-1-dependent proliferation and beta-catenin/cyclinD1

165 43.2%, normalizing in each case at 1 month (CSF 1.51 +/- 0.28 %W; P = .001; range 1.14-2.00 %W), 3 m

166 Furthermore, we uncovered a multistep CSF-1-dependent systemic mechanism central to lupus neph

167 Notably, CSF-1 treatment increased TEC proliferation and reduced

168 d suppressed proliferation in the absence of CSF-1, but restored most of the CSF-1-stimulated prolife

169 In the absence of CSF-1, pregnant mice were more susceptible to uterine in

170 yeloid cells in RT2 tumors in the absence of CSF-1.

171 Indeed, addition of CSF-1 or IL-34 to microglia-free, CSF-1R-expressing dors

172 constraints mediated by the availability of CSF-1.

173 ated, rising >6-fold in vivo after 2 days of CSF-1 treatments.

174 dent renal repair, we assessed the effect of CSF-1 on I/R in mice in which CD11b+ cells were genetica

175 the hypothesis that amplified expression of CSF-1 detected in the serum or urine correlates with int

176 with a concomitant increase in expression of CSF-1 mRNA and protein.

177 We suggest that inclusion of CSF-1 as part of any vaccination regimen against HSV inf

178 ata show for the first time the induction of CSF-1 and c-fms in cervical carcinomas and suggest that

179 otein interaction resulting in inhibition of CSF-1 transcription.

180 at the cell-surface and secreted isoforms of CSF-1 have opposing effects on macrophage activation and

181 act of cell-surface and secreted isoforms of CSF-1 on macrophage-related disease in connexin32-defici

182 -559 alone (Y559AB) supported a low level of CSF-1-independent proliferation that was slightly enhanc

183 (Y291F mutation) did not reduce the level of CSF-1-induced WASP activation.

184 ey disease in mice with the highest level of CSF-1.

185 as(lpr) strains expressing varying levels of CSF-1 (high, intermediate, none), and use of an ex vivo

186 In humans, we found increased levels of CSF-1 in the serum, urine, and kidneys of patients with

187 The observed loss of CSF-1 appeared to be caused by a more proximal deficienc

188 onment in the kidney to release mediators of CSF-1, CSF-1R, and epidermal growth factor expression in

189 of this study is to explore the presence of CSF-1 and IL-34 in whole saliva in relation to periodont

190 tor-specific Smad-dependent transcription of CSF-1, osterix, and BMP-2.

191 However, the effect of BMP-2 on CSF-1 expression has not been studied.

192 low level of self-replication, and depend on CSF-1.

193 he maternal decidual tissue are dependent on CSF-1-regulated macrophages.

194 We determined the effect of PDGF on CSF-1 expression using MEOE-3M ameloblasts as a model.

195 proliferation above homeostatic levels, only CSF-1 led to the recruitment of monocytes and neutrophil

196 M-CSF (or CSF-1) and GM-CSF can regulate the development and funct

197 trusions (ruffles), which showed that FKN or CSF-1 stimulated strong transient ruffling in both LR5 c

198 The chemotactic response to FKN or CSF-1 was quantitated by measurement of the formation of

199 results imply that the inhibition of FKN- or CSF-1-stimulated cell ruffling was a direct consequence

200 Abl regulated BMP-2-induced osteoclastogenic CSF-1 expression.

201 ce that BMP-2 increases the osteoclastogenic CSF-1 expression by a transcriptional mechanism using th

202 Unexpectedly, a parallel CSF-1-regulated, but CCR2-independent pathway influenced

203 In the periphery, CSF-1 regulates the migration, proliferation, function,

204 In bone marrow-derived precursors, CSF-1 alone promoted assembly of MITF-PU.1 complexes at

205 ncreasing the level of secreted proteoglycan CSF-1 in serum amplifies renal inflammation; and 4) cell

206 C-TAK1 interaction was disrupted by RANKL/CSF-1 treatment.

207 om cytoplasm to nucleus dependent upon RANKL/CSF-1 action.

208 beta1 is inhibited by blocking EGF receptor, CSF-1 receptor, or macrophage function, indicating that

209 Recombinant CSF-1, antibodies against the ligand and the receptor, a

210 contact is required for Mphi to up-regulate CSF-1-dependent expression of IFN-gamma.

211 -BB increased DNA synthesis and up-regulated CSF-1 mRNA and protein in MEOE-3M.

212 PDGF stimulates DNA synthesis and regulates CSF-1 in these cells.

213 Salivary CSF-1, IL-34, and matrix metalloproteinase (MMP)-8, a bi

214 tal treatment, whereupon changes in salivary CSF-1, IL-34, and MMP-8 levels were determined and relat

215 hage-dependent invasion, tumor cells secrete CSF-1 and sense EGF, whereas the macrophages secrete EGF

216 e cell surface or precursors of the secreted CSF-1 isoforms for Mphi accumulation, activation, and Mp

217 bstantially more effective than the secreted CSF-1 isoforms; 2) the chondroitin sulfate glycosaminogl

218 eatment of Pten null mice with the selective CSF-1 receptor inhibitor GW2580 decreases MDSC infiltrat

219 hereas the macrophages secrete EGF and sense CSF-1.

220 cking patients, we found that elevated serum CSF-1 heralded the initial onset of disease, and a rise

221 lony-stimulating factor-1 (CSF-1)-stimulated CSF-1 receptor (CSF-1R) tyrosine phosphorylation initiat

222 Probing further, UVB stimulates CSF-1 expression by keratinocytes leading to recruitment

223 al inflammatory response, and exhibit strict CSF-1 dependence for growth.

224 onfers sufficient kinase activity for strong CSF-1-independent proliferation, whereas Tyr-559 maintai

225 capillary guidance role for locally supplied CSF-1.

226 We report that 1) cell surface CSF-1 isoform is sufficient to restore Mphi accumulation

227 for amelogenesis, and ameloblasts synthesize CSF-1.

228 Systemic CSF-1 skewed the frequency of monocytes toward "inflamma

229 Here, we found that increasing systemic CSF-1 hastened the onset of lupus nephritis in MRL-Fas(l

230 that express high, moderate, or no systemic CSF-1, we detected a much higher tempo of kidney disease

231 eduction of macrophages and whether systemic CSF-1, as opposed to intrarenal CSF-1, promotes macropha

232 elopment of cGVHD and suggest that targeting CSF-1 signaling after transplantation may prevent and tr

233 rthermore, our findings imply that targeting CSF-1/CSF-1R signaling may be therapeutically effective

234 , our results illuminate a Kindlin-2/TGFbeta/CSF-1 signaling axis employed by breast cancer cells to

235 exhibited a broader regional expression than CSF-1, mostly without overlap.

236 vels of select restriction factor genes than CSF-1-Mphis.

237 We conclude that CSF-1 promotes a resident-type macrophage phenotype.

238 We conclude that CSF-1 promotes angiogenesis at the chondroosseous juncti

239 CSF1R signaling, GW2580, to demonstrate that CSF-1 regulates the tumor recruitment of CD11b(+)Gr-1(lo

240 These findings demonstrated that CSF-1-mediated expansion and polarization of resident re

241 iver CSF-1 intradermally, we determined that CSF-1 induces CLE in lupus-susceptible MRL-Fas(lpr) mice

242 rrow chimeric mice, we have established that CSF-1 receptor-deficient hematopoietic precursors failed

243 We therefore tested the hypothesis that CSF-1 is central to tubular repair using an acute renal

244 Thus the results indicate that CSF-1-mediated receptor dimerization leads to a Tyr-559/

245 with the convenient AIP model indicated that CSF-1 neutralization led to a relatively uniform reducti

246 mulating factor-1 (CSF-1) gene, we show that CSF-1-dependent macrophage functions are required for th

247 Postnatal neocortical expression showed that CSF-1 was expressed in layer VI, whereas IL-34 was expre

248 Taken together, these data suggest that CSF-1 mediates renal repair by both a macrophage-depende

249 ility compared with control, suggesting that CSF-1/c-fms signaling may be involved in enhanced surviv

250 The CSF-1 receptor (CSF-1R) is a tyrosine kinase that is tar

251 The CSF-1 receptor (CSF-1R) regulates CNS microglial develop

252 ic and pharmacologic approaches to block the CSF-1/CSF-1R signaling result in a significant alleviati

253 an breast tumors, the expression of both the CSF-1 ligand and its receptor in tumor cells leads to a

254 sed to restore osteoclast populations in the CSF-1-null toothless (csf1(tl)/csf1(tl)) osteopetrotic r

255 One example is the CSF-1 receptor (CSF-1R, CD115, c-fms), which is used as

256 We used an inhibitor of the CSF-1 receptor (CSF-1R) to target TAMs in a mouse proneu

257 in vivo and establish the importance of the CSF-1 receptor in this process.

258 ated messenger RNAs revealed that 80% of the CSF-1-regulated canonical miR-21 targets are proinflamma

259 e absence of CSF-1, but restored most of the CSF-1-stimulated proliferation.

260 potential clinical uses of modulators of the CSF-1/CSF-1R system.

261 F-1 signaling, PLCgamma1 is recruited to the CSF-1 receptor following exposure to the cytokine.

262 r NOD mice with a monoclonal antibody to the CSF-1 receptor resulted in depletion of the resident mac

263 his restraint and may also contribute to the CSF-1-regulated proliferative response by activating Src

264 SFK) signaling is sufficient to transmit the CSF-1 lineage instructive signal.

265 by in vivo macrophage suppression using the CSF-1 receptor kinase inhibitor GW2580.

266 ia depletion, via treatment of mice with the CSF-1 receptor antagonist PLX5622, and abrogated neurona

267 d positively with CSF-1, MMP-8, and with the CSF-1/IL-34 ratio, and negatively with IL-34 in patients

268 together, these data suggest that the three CSF-1 isoforms have distinct biologic properties, sugges

269 tion may have developed as an alternative to CSF-1 to increase resident MPhi numbers without coincide

270 of IL-10 receptor (IL-10R) was equivalent to CSF-1 neutralization in enhancing primary tumor response

271 alization to the periphery after exposure to CSF-1 for 2.5 min was shown by immunofluorescence micros

272 07 alone to the YEF backbone (Y807AB) led to CSF-1-independent but receptor kinase-dependent prolifer

273 determine the contribution of macrophages to CSF-1-dependent renal repair, we assessed the effect of

274 icient for both proteins and, in response to CSF-1 stimulation, Abr and Bcr transiently translocated

275 ptor ligands by uterine Mphis in response to CSF-1.

276 Taken together, CSF-1 is envisioned as the match and lupus susceptibilit

277 tion with LPS, migrated inefficiently toward CSF-1 and CCL2.

278 Confirming the specificity toward CSF-1 signaling, PLCgamma1 is recruited to the CSF-1 rec

279 After treatment CSF-1 and MMP-8 levels decreased together with observed

280 As a treatment, CSF-1 has therapeutic potential in tissue repair.

281 Furthermore, serum and urine CSF-1 levels correlated with lupus activity, and intrare

282 Moreover, an elevation in serum or urine CSF-1 levels correlated with increasing intrarenal CSF-1

283 We found increased serum or urine CSF-1 levels in patients with cutaneous, serositis, and

284 rial monitoring for a rise in serum or urine CSF-1 levels in patients with SLE reflects kidney histop

285 set of disease, and a rise in serum or urine CSF-1 predicted recurrences of LN before clinical eviden

286 In vitro, CSF-1 stimulation resulted in rapid autophosphorylation

287 In vivo CSF-1-induced WASP activation was fully Cdc42-dependent.

288 , lacks in vitro kinase activity and in vivo CSF-1-regulated tyrosine phosphorylation.

289 ene expression changes in long bone RNA when CSF-1 injections were used to restore osteoclast populat

290 Whereas CSF-1 injections quickly restore endosteal osteoclast po

291 Here, we address which CSF-1-activated pathways are involved in transmitting th

292 eceptor was upregulated and coexpressed with CSF-1 in TECs following renal injury in mice and humans.

293 al macrophages, observations consistent with CSF-1 signaling being essential only at a relatively lat

294 Mice injected with CSF-1 following I/R exhibited hastened healing, as evide

295 Conversely, injection of mice with CSF-1 DNA, which enhances the development of M2 macropha

296 dontal parameters correlated positively with CSF-1, MMP-8, and with the CSF-1/IL-34 ratio, and negati

297 Cells transfected with CSF-1 promoter deletion constructs were analyzed.

298 ent of recipients after transplantation with CSF-1 exacerbated macrophage infiltration and cutaneous

299 vation of WASP in response to treatment with CSF-1 was also shown to be phosphatidylinositol 3-kinase

300 and wild-type littermates, with and without CSF-1 treatment, at 2 weeks, before the dysplasia is pro