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 and IL-34 secretion from GF was evaluated in respo

6 CSF-1 and IL-34 were expressed and secreted constitutive

7 CSF-1 deficiency decreased macrophage infiltration by ap

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

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

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

11 CSF-1 heightened monocyte proliferation in the bone marr

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

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

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

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

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

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

18 CSF-1 was increased in gingival tissue from periodontiti

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

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

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

22 Colony-stimulating factor 1 (CSF-1) and interleukin (IL)-34 are important for the fun

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

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

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

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

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

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

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

30 gands IL-34 and colony stimulating factor 1 (CSF-1).

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

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

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

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

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

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

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

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

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

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

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

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

43 Colony stimulating factor-1 (CSF-1) promotes placentation and creates a pro-inflammat

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

45 h low levels of colony-stimulating factor-1 (CSF-1), inhibit their differentiation into macrophages.

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

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

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

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

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

51 (TGCT), are rare colony stimulating factor-1(CSF-1)-driven proliferative disorders affecting joints.

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

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

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

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

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

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

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

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

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

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

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

63 c CSF-1R kinase inhibitor, GW2580, abolishes CSF-1 induced trophoblast cell proliferation and migrati

64 Accordingly, CSF-1 depletion from Nestin(+) cells led to severe deple

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

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

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

68 hen demonstrate the expression of CSF-1R and CSF-1 in the cytotrophoblast and syncytiotrophoblast wit

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

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

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

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

73 atment, mRNA and protein levels of CSF1R and CSF-1 were significantly increased.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

107 1 (CSF-1) can induce invasion through an EGF/CSF-1 paracrine loop between cancer cells and macrophage

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

125 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 ial identity was driven by the CSF-1R ligand CSF-1, independently of the alternate CSF-1R ligand, IL-

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

161 F-1 receptor (CSF-1R) as well as its ligand (CSF-1) in immortalised first trimester trophoblast cells

162 nd that mRNA expression of the CSF1R ligand, CSF-1, is increased in the brain of PD patients compared

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

164 eptor (CSF-1R), which has two known ligands: CSF-1 and interleukin-34 (IL-34).

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

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

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

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

169 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

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

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

172 These findings reveal a novel CSF-1-CSF-1R signaling-mediated mechanism that contribut

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

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

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

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

177 constraints mediated by the availability of CSF-1.

178 suggests that pharmacological disruption of CSF-1/CSF-1R signaling axis could be the basis of a new

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

180 The expression of CSF-1 and IL-34 in gingival tissue and fibroblasts sugge

181 this study is to evaluate the expression of CSF-1 and IL-34 in gingival tissue and gingival fibrobla

182 Expression of CSF-1 and IL-34 in gingival tissue was assessed by weste

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

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

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

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

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

188 -559 alone (Y559AB) supported a low level of CSF-1-independent proliferation that was slightly enhanc

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

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

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

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

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

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

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

196 c-LPS, or Pg-LPS, increased the secretion of CSF-1 (P < 0.05) and Ec-LPS stimulation increased IL-34

197 lammatory stimuli increased the secretion of CSF-1 and IL-34 with comparable levels measured from GF

198 thelial cells (LECs) were the main source of CSF-1 within the lymph node and conditional deletion of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 Strikingly, CSF-1 deficiency and alteration of cerebellar microglia

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

226 capillary guidance role for locally supplied CSF-1.

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

243 We hypothesised that CSF-1 is also involved in the placentation and maintenan

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 Our data suggests that CSF-1 is involved in the survival and proliferation of t

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

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

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

254 Imatinib mesylate (IM) blocks the CSF-1 receptor.

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

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

257 we demonstrate the immunolocalisation of the CSF-1 receptor (CSF-1R) as well as its ligand (CSF-1) in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

273 07 alone to the YEF backbone (Y807AB) led to CSF-1-independent but receptor kinase-dependent prolifer

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

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 Whereas CSF-1 injections quickly restore endosteal osteoclast po

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

291 While CSF-1 has been extensively studied, the biology and func

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