ライフサイエンスコーパス: CX3CR1

1 SC enriched for effector genes (Gzmb, Klrg1, Cx3cr1).

2 ns is dependent on the fractalkine receptor (CX3CR1).

3 acks expression of the fractalkine receptor (CX3CR1).

4 nds to the corresponding chemokine receptor, CX3CR1.

5 g and is independent of its interaction with CX3CR1.

6 omeruli using beta2 and alpha4 integrins and CX3CR1.

7 is significantly improved in the absence of CX3CR1.

8 ractalkine (CX3CL1), an endogenous ligand of CX3CR1.

9 r macrophages express the chemokine receptor CX3CR1.

10 upon expression of the fractalkine receptor CX3CR1.

11 ave increased expression of CCR1, CXCR3, and CX3CR1.

12 mmatory OCLs (i-OCLs), part of which express Cx3cr1.

13 teractions with the human chemokine receptor CX3CR1.

14 AGM was dependent on the chemokine receptor Cx3cr1.

15 ated CNS-myeloid exhibited downregulation of Cx3cr1.

16 naling function through binding its receptor CX3CR1.

17 10R, CD206, and CCR2 but little TNF-alpha or CX3CR1.

18 myeloid cells expressing HLA-DR, CD11c, and CX3CR1.

19 CX3CR1, a cell surface marker whose expression is associ

20 Deletion of one allele of CX3CR1, a chemokine receptor, limited infiltration of pe

21 Together, these data indicate that CX3CR1, a microglia-specific chemokine receptor, is a no

22 Published data show that genetic deletion of CX3CR1, a microglia-specific chemokine receptor, promote

23 Modulation of CX3CR1 activation in septic mice controlled monocyte adh

24 1 signalling and suggest that an increase of CX3CR1 activity contributes to the attenuated inflammato

25 ch that the number of lesions decreased when CX3CR1 activity increased.

26 tosis mice) and genetic ablation of CCR2 and CX3CR1 all inhibited LLC1 tumor growth and metastasis, s

27 nt with these results, the pro-adhesive I249 CX3CR1 allele in humans was associated with a lower inci

28 in signaling suppressor DKK1, or knockout of CX3CR1 alleviated gp120-induced mechanical allodynia in

29 are orchestrated by the chemokine receptors CX3CR1 and CCR2 and their cognate ligands.

30 ower levels of F4/80 and chemokine receptors CX3CR1 and CCR2 in the F4/80(+) renal resident macrophag

31 ry, microglial activation, and signaling via CX3CR1 and CCR2 receptors, or following direct TLR2 stim

32 vision loss at P31 (B2m, Tlr 2, 3, 4, C1qa, Cx3cr1 and Fas).

33 ess the vascular endothelium-homing receptor CX3CR1 and migrate toward CX3CL1-expressing endothelial

34 ted the expression of the chemokine receptor CX3CR1 and the integrin alpha4beta7 on CD8 T cells prime

35 ases, we found a significant upregulation of CX3CR1 and TMEM119 mRNA expression and a downregulation

36 are associated with the expression level of CX3CR1 and TNFAIP1, and affect the transcription factor

37 retina nor pigmentation, although peripheral CX3CR1(+) and CCR2(+) monocytes infiltrate the optic ner

38 We showed that Cx3cr1(+) and Cx3cr1(neg) i-OCLs differ considerably in

39 e, we investigated the contribution of mouse Cx3cr1(+) and Cx3cr1(neg) i-OCLs to bone loss.

40 and their corresponding Teff precursors were CX3CR1(-) and CX3CR1(high), respectively.

41 Finally, inhibition of ADAM10 phenocopies Cx3cr1(-/-) and Cx3cl1(-/-) synapse elimination defects.

42 and expressed markers of endothelial homing (CX3CR1) and cytotoxicity (NKG2D and perforin).

43 in the promoters of 4 genes, NLRC5, TRIM69, CX3CR1, and BCL9, in the discovery sample and in meta-an

44 t migration to inflamed sites, such as CCR2, CX3CR1, and CCR5, in TPH cells.

45 cell-associated genes, including CD1, FLT3, CX3CR1, and CCR6 Each clade, and each member of both cla

46 hese cells expressed monocytic markers Ly6C, CX3CR1, and CD115, suggesting monocytic origin.

47 s at P22, including beta-2 microglobulin and Cx3cr1, and during vision loss at P31 (B2m, Tlr 2, 3, 4,

48 phenotypic markers, including CD11b, IBA-1, CX3CR1, and P2RY12, and phagocytosed micron-size super-p

49 Among them, ITGAV, FoxC1, and CX3CR1 are significantly enriched in patients with 2 or

50 le depletion of resident macrophages using a Cx3cr1-based system led to impaired cardiac function and

51 Lack or low levels of expression of CX3CL1-CX3CR1 by tumor cells identifies a group of CRC patients

52 emia-reperfusion triggered marked unilateral CX3CR1-CCR2 dependent accumulation of diverse leukocyte

53 2 stimulation, in both models, disruption of CX3CR1-CCR2 signaling attenuated both monocyte and neutr

54 ting myeloid cells with intact and disrupted CX3CR1-CCR2 signaling could identify novel therapeutic t

55 Disrupted CX3CR1-CCR2 signaling was neuroprotective in part by att

56 eability, injury, microglial activation, and CX3CR1-CCR2 signaling, focusing on the dynamics early af

57 We report that CX3CR1-CCR2-mediated myeloid cell recruitment contribute

58 gand 1 (PD1-L1), CxxxC chemokine receptor 1 (Cx3CR1), CCR7, and CCR9.

59 tly increased the expression levels of iNOS, CX3CR1, CD206, phospho-STAT1 and phospho-STAT3 proteins

60 displayed high ex vivo levels of granzyme B, CX3CR1, CD38, or HLA-DR but less often coexpressed CD38(

61 T recipients and is particularly elevated on CX3CR1(+) CD8(+) T cells, suggesting that these cells co

62 These data showed that the rapidly deployed CX3CR1(+) cell-based mechanism of immune exclusion is a

63 Salmonella Typhimurium infection, intestinal CX3CR1(+) cells can either extend transepithelial cellul

64 antly reduced after the adoptive transfer of CX3CR1(+) cells directly into the intestinal lumen, cons

65 antly reduced after the adoptive transfer of CX3CR1(+) cells directly into the intestinal lumen, cons

66 g real-time in vivo imaging we observed that CX3CR1(+) cells migrated into the lumen moving through p

67 testinal lumen, consistent with intraluminal CX3CR1(+) cells preventing S.

68 testinal lumen, consistent with intraluminal CX3CR1(+) cells preventing S. Typhimurium from infecting

69 l relevance of the intraluminal migration of CX3CR1(+) cells remained to be determined.

70 conclusion, tumoral expression of the CX3CL1-CX3CR1 chemokine axis functions as a retention factor, i

71 However, whether CX3CR1 confers protection against mucosal C. albicans in

72 Since RSV binding to CX3CR1 contributes to disease pathogenesis, we investiga

73 RSV binding to CX3CR1 contributes to disease pathogenesis; therefore, w

74 The chemokine receptors CCR2, CCR5, and CX3CR1 coordinate monocyte trafficking in homeostatic an

75 High expression of CX3CR1 correlates with significantly shorter survival, s

76 Interventions that specifically target CX3CR1 could reduce the adverse effects of inflammation

77 ly in microglia (Cx3cr1(CreER);Mecp2(fl/y)or Cx3cr1(Cr)(eER); Mecp2(LSL/y)) had little effect on exce

78 g Raptor loxed (Raptor(flox/flox)) mice with CX3CR1(CreER) mice, which express Cre recombinase under

79 Mecp2 expression specifically in microglia (Cx3cr1(CreER);Mecp2(fl/y)or Cx3cr1(Cr)(eER); Mecp2(LSL/y

80 deletion of TSPO in resident microglia using Cx3cr1(CreERT2):TSPO(fl/fl) mice or targeting the protei

81 e tracing studies-labelling cells expressing Cx3cr1, Csf1r or Flt3-to identify the precursors of oste

82 f resident arterial macrophages depends on a CX3CR1-CX3CL1 axis within the vascular niche.

83 inoma) caused up-regulation of CCR2/CCL2 and CX3CR1/CX3CL1 in both the cancer cells and the MPhi.

84 s rapidly differentiate into BMRMs, with the CX3CR1/CX3CL1 signaling axis being essential for the mai

85 ophage phagocytosis function was impaired by CX3CR1 deficiency as demonstrated by increased number of

86 ntry into the lung parenchyma by half, while CX3CR1 deficiency doubles it.

87 sually causes fibrosis, we hypothesized that CX3CR1 deficiency should attenuate renal fibrosis.

88 r and subset composition were not altered by CX3CR1 deficiency.

89 hat in the presence of inflammatory stimuli, CX3CR1-deficient (CX3CR1(-/-)) microglia and macrophages

90 IGF-1 (-53%), and IL-6 (-40%) was reduced in CX3CR1-deficient macrophages as compared with WT control

91 Stable patrolling is unaffected in CX3CR1-deficient mice and involves the contribution of L

92 We have previously shown that Cx3cr1-deficient mice develop age- and stress- related s

93 CX3CR1-deficient mice exhibited significantly lower expr

94 In this study, we show that CX3CR1-deficient mice fail to resolve gut inflammation d

95 ng and flow cytometry revealed in kidneys of CX3CR1-deficient mice more motile Ly6C/Gr-1(+) macrophag

96 ble for increased photoreceptor apoptosis in Cx3cr1-deficient mice, has not been elucidated.

97 However, in CX3CR1-deficient mice, the clearance of myelin debris by

98 concomitantly with reduced contacts between Cx3cr1-deficient microglia and abGCs' dendritic shafts,

99 Here we show that Cx3cr1-deficient MPs express increased surface P2X7 rece

100 Cx3cr1-deficient MPs have been shown to increase neurona

101 reason for increased IL-1beta secretion from Cx3cr1-deficient MPs, and whether IL-1beta is responsibl

102 Data in the current manuscript indicate that CX3CR1 deletion changes microglia and macrophage functio

103 ey reside through CX3C-chemokine receptor 1 (CX3CR1)-dependent adherence.

104 have a protective effect during sepsis via a CX3CR1-dependent adhesion mechanism.

105 this monocyte deployment is controlled by a CX3CR1-dependent balance between marginating and circula

106 Here, we tested the hypothesis that CX3CR1-dependent changes in microglia and macrophage fun

107 results provide an explanation for increased CX3CR1-dependent IL-1beta secretion and suggest that IL-

108 renal vascular wall in a chemokine receptor CX3CR1-dependent manner.

109 Indeed, limiting CX3CR1-dependent signaling could improve rehabilitation

110 ocyte-enriched bone marrow cells into septic Cx3cr1-depleted mice prevented kidney damage and promote

111 Cx3cr1-driven deletion of Nrros shows its crucial role i

112 e mice, CX3CR1(gfp/gfp), CX3CR1(gpf/wt), and CX3CR1-DTR-EYFP.

113 To investigate the impact of CX3CR1 elevation in vivo, we compared LPS-induced inflam

114 ighly polarized, with a strong bias toward a CX3CR1(+) Eomesodermin(+) perforin(+) granzyme B(+) CD45

115 y reduced numbers of nonclassical monocytes (CX3CR1(-/-)) exhibited a significant reduction in neutro

116 Inducible ablation of IL-1R1 in CX3CR1-expressing cells eliminated cognitive impairment

117 ytometry demonstrated a 4.5-fold increase in CX3CR1-expressing immune cells (p <= 0.0001), including

118 to liver was dramatically reduced in CX3CL1-CX3CR1-expressing tumors, and ligand-receptor interactio

119 ages were observed that differed in terms of CX3CR1 expression and migratory capacity.

120 Lack of Cx3cr1 expression was associated with significantly alte

121 5 promotes the cytotoxic phenotype, elevates CX3CR1 expression, and enhances the trafficking of CD57(

122 In correlation with the enhanced CX3CR1 expression, Lrrk2-null microglia migrated faster

123 ciency diminishes CX3C chemokine receptor 1 (CX3CR1) expression and vascular endothelial growth facto

124 ess the vascular endothelium-homing receptor CX3CR1 (fractalkine receptor) are enriched in HIV-infect

125 enic mice expressing single mutations in the Cx3cr1, GDNF and CCR2 genes.

126 CX3CR1 gene deletion or anti-Abeta immunotherapy causes

127 oded macrophages (Ccr2 (RFP)) and microglia (Cx3cr1 (GFP)).

128 Apoe(-/-) Cx3cr1(GFP) Cd11c(YFP) mice have 4 groups of macrophages

129 Intrascrotal administration of Gal-3 to CX3CR1(gfp/+) mice confirmed that approximately equal nu

130 tion of wild-type (C57BL/6), Gal-3(-/-), and CX3CR1(gfp/+) mice were assessed by intravital microscop

131 gondii infection of C57BL/6J and CCR2(RFP/+)CX3CR1(GFP/+) mice.

132 s, depletion of microglia before tMCAO in P9 Cx3cr1(GFP/+)/Ccr2(RFP/+) mice exacerbated injury and in

133 Muscle injury repair was delayed in CX3CR1(GFP/GFP) mice as compared with wild-type (WT) con

134 gocytosed beads within macrophages (-15%) in CX3CR1(GFP/GFP) mice as compared with WT controls.

135 al fecal load in CX3CR1(+/gfp) compared with CX3CR1(gfp/gfp) mice following oral infection.

136 nd mouse MPs in vitro and inflammation-prone Cx3cr1(GFP/GFP) mice in vivo, we demonstrate that MP-der

137 CD11c-EYFP, CD11c-EYFP-DTR, germ-free mice, CX3CR1(gfp/gfp), CX3CR1(gpf/wt), and CX3CR1-DTR-EYFP.

138 261-induced mouse models in combination with CX3CR1(GFP/WT);CCR2(RFP/WT) double knock-in mice.

139 upported by a higher bacterial fecal load in CX3CR1(+/gfp) compared with CX3CR1(gfp/gfp) mice followi

140 A similar increase is seen in CX3CR1(+/GFP)/apoE(-/-) mice on chow diet, with a furthe

141 scopy of unrestrained large arteries in live CX3CR1-GFP (green fluorescent protein) mice, we show tha

142 icroscopy in ex vivo spinal cord slices from CX3CR1-GFP mice complemented with confocal analyses of C

143 exes) that allow visualization of microglia (CX3CR1-GFP) and infiltrating peripheral myeloid cells (C

144 c-EYFP-DTR, germ-free mice, CX3CR1(gfp/gfp), CX3CR1(gpf/wt), and CX3CR1-DTR-EYFP.

145 lly matured NK cells with high expression of CX3CR1, HAVCR2 (TIM-3), and ZEB2 represents terminally d

146 he striatum of Lrrk2(-/-) knockout mice with Cx3cr1 heterozygous and homozygous knockout background.

147 nfection, CXCR3(hi) CX3CR1(lo) and CXCR3(lo) CX3CR1(hi) CD8 T cells localize to different compartment

148 changes of Ly6C(pos)CX3CR1(lo) and Ly6C(neg)CX3CR1(hi) macrophage populations during skeletal muscle

149 mmune suppressive function of the regulatory CX3CR1(hi) macrophages (Mvarphi), which express the high

150 t cells and increased phagocytosis of OVA by CX3CR1(hi) macrophages.

151 CX3CR1(hi) monocyte/macrophages promote P. gingivalis su

152 ally, TRPV1(-/-) or CB2(-/-) mice have fewer CX3CR1(hi) Mvarphi in the gut.

153 T cells acquired an effector-like CXCR3(lo) CX3CR1(hi) phenotype in the absence of B cells.

154 cruitment and differentiation to Ly6C(hi) vs CX3CR1(hi) subsets, respectively.

155 ssical, patrolling, or alternative (CCR2(low)CX3CR1(hi)) monocytes.

156 tioned to CX3CR1(Hi)CCR2(Lo) macrophages and CX3CR1(Hi)CCR2(-) microglia-like cells.

157 uited to the GBM, where they transitioned to CX3CR1(Hi)CCR2(Lo) macrophages and CX3CR1(Hi)CCR2(-) mic

158 tioned, in situ, from CCR2(hi)Cx3CR1(low) to CX3CR1(hi)CCR2(low) within the ringlike structure and th

159 Taken together, our results highlight CX3CR1(high) monocytes and TNF-alpha as potential therap

160 RATIONALE: Nonclassical mouse monocyte (CX3CR1(high), Ly-6C(low)) patrolling along the vessels o

161 esponding Teff precursors were CX3CR1(-) and CX3CR1(high), respectively.

162 Furthermore, activation of CX3CR1(high)Ly6C(low) monocytes impaired motor learning

163 Although Cx3cr1(+) i-OCLs are associated with inflammation, they

164 Here, we found that the chemokine receptor CX3CR1 identifies three distinct CD8(+) Teff and Tmem su

165 pp65; MDSC depletion further augmented CD4(+)CX3CR1(+)IFNgamma(+) cells and IFNgamma production.

166 CMV(+) controls exhibit an increase in CD4(+)CX3CR1(+)IFNgamma(+) cells in response to CMVpp65; MDSC

167 CMVpp65 specific CD4(+)CX3CR1(+)IFNgamma(+) cells were also decreased in presen

168 We showed an increased expression of CX3CR1 in all monocyte subpopulations and of CCR2 and CC

169 Our results demonstrate that loss of Cx3cr1 in CNS-myeloid triggers a Cxcl10-mediated vicious

170 Transduction of CX3CL1 and CX3CR1 in CRC tumor cell lines induced cell aggregation

171 protein (GFAP), and the fractalkine receptor CX3CR1 in DRGs.

172 establish an essential role for the receptor CX3CR1 in gut macrophages in resolving inflammation in t

173 a, CCL20, and CCL8, and higher expression of CX3CR1 in monocytes from old subjects.

174 results highlight the crucial role played by CX3CR1 in myelin removal and show that there can be no e

175 We studied the role of CX3CR1 in regulating intramuscular macrophage number and

176 x3cl1) and chemokine receptors (Ccr6, Cxcr6, Cx3cr1) in livers of Tnfr1(-/-)/Mdr2(-/-) mice indicated

177 support a role for the fractalkine receptor (CX3CR1) in the initiation of peritoneal adhesion importa

178 ered that a defect in the chemokine receptor CX3CR1 increases susceptibility of mice and humans to sy

179 d in hyperlipidemia and atherosclerosis in a CX3CR1-independent fashion and plays a potential role in

180 at responds to G-CSF by engaging Cathepsin S-CX3CR1-inducible NOS signaling.

181 Thus, CX3CR1 inhibition should be avoided in DC-independent in

182 Both Tcm and CX3CR1(int) cells homed to lymph nodes, but CX3CR1(int)

183 CX3CR1(int) cells homed to lymph nodes, but CX3CR1(int) cells, and not Tem cells, predominantly surv

184 infection also induced a numerically stable CX3CR1(int) subset that represented approximately 15% of

185 As CX3CR1(int) Tmem cells present unique phenotypic, homeos

186 CX3CR1(int) Tmem cells underwent more frequent homeostat

187 that neuron-to-microglial communication via CX3CR1 is an essential component of visual cortical deve

188 Intravital microscopy revealed that CX3CR1 is critical for Ly6Clo monocyte transmigration ac

189 ng two different mouse models, we found that Cx3cr1 is dispensable for the induction of interleukin 1

190 We conclude that CX3CR1 is important to acute skeletal muscle injury repa

191 own that the microglial fractalkine receptor CX3CR1 is involved in synaptic development and hippocamp

192 t signaling through the fractalkine receptor CX3CR1 is not an essential component in the mechanisms o

193 Taken together, these data indicate that CX3CR1 is not essential for protection of the host again

194 Our data show that CX3CR1 is not required for normal development of V1 resp

195 a and suppress M. tuberculosis growth, while CX3CR1(+) KLRG1(+) Th1 cells accumulate in the lung vasc

196 Cx3cr1 knockout in CNS-myeloid increased br-met incidenc

197 10 knockout mice parabiosed with miR-210 WT; Cx3cr1 knockout mice (deficient in myeloid recruitment)

198 Female Cx3cr1 knockout mice develop 'male-like' hypothalamic mi

199 Furthermore, CX3CR1 knockout mice resist bone resorption in the oral

200 n of gastric monocyte infiltration using the Cx3cr1 knockout mouse model prevented SPEM development.

201 ale mice fed a high-fat diet maintain CX3CL1-CX3CR1 levels while male mice show reductions in both li

202 ing a respiratory virus infection, CXCR3(hi) CX3CR1(lo) and CXCR3(lo) CX3CR1(hi) CD8 T cells localize

203 dscape of transcriptomic changes of Ly6C(pos)CX3CR1(lo) and Ly6C(neg)CX3CR1(hi) macrophage population

204 ly GR1(+), Ly6c(hi), CCR2(hi), CCL2(hi), and CX3CR1(lo) In addition, expression of F4/80 and the recr

205 Using this approach, we demonstrated that CX3CR1(Lo)CCR2(Hi) monocytes were recruited to the GBM,

206 We observed that the CCR2(hi)CX3CR1(low) monocytes were recruited early and persisted

207 onocytes transitioned, in situ, from CCR2(hi)Cx3CR1(low) to CX3CR1(hi)CCR2(low) within the ringlike s

208 cytes: classical or proinflammatory (CCR2(hi)CX3CR1(low)) and nonclassical, patrolling, or alternativ

209 flammatory (CCR2(+)Ly6C(hi)) and patrolling (CX3CR1(+)Ly6C(lo)) monocytes into the blood and brain du

210 naling blockade, resulting in recruitment of CX3CR1+Ly6Clo monocytes into the tumor.

211 +) T cells clustered with CD4(+) T cells and CX3CR1(+) macrophages and/or dendritic cells around area

212 e intestines in steady-state that intestinal CX3CR1(+) macrophages form an interdigitated network int

213 the accumulation of CD11b(+)F4/80(hi)CD64(+)CX3CR1(+) macrophages in the gastric lamina propria.

214 CX3CR1(+) macrophages in the intestinal lamina propria c

215 similar regional accumulation of CCR2(+) and CX3CR1(+) macrophages, and provided functional rejuvenat

216 ut reside and are activated in apposition to CX3CR1(+) macrophages.

217 mporal and regional induction of CCR2(+) and CX3CR1(+) macrophages.

218 ic fatty liver disease, we hypothesized that CX3CR1 may influence the development of steatohepatitis.

219 he therapeutic strategy of blocking CCR2 and CX3CR1 may prove beneficial for halting lung cancer prog

220 hus suggest that, under chronic pain states, CX3CR1-mediated activation of microglia drives the facil

221 murium strain that specifically targeted the CX3CR1-mediated entry route.

222 murium strain that specifically targeted the CX3CR1-mediated entry route.

223 ains differing in their ability to carry out CX3CR1-mediated sampling and intraluminal migration.

224 Also, we reported that the absence of CX3CR1-mediated sampling did not affect Ab responses to

225 Also, we reported that the absence of CX3CR1-mediated sampling did not affect Ab responses to

226 V/CMV coinfection and in atherosclerosis via CX3CR1-mediated trafficking and CD2/LFA-3-mediated costi

227 AngII/Cx3cr1(-/-) mice also showed an M1 phenotypic shift rela

228 Cohousing of wild-type and CX3CR1(-/-) mice during the AOM/DSS treatment attenuated

229 t, in sampling-deficient/migration-deficient CX3CR1(-/-) mice the numbers of S.

230 t, in sampling-deficient/migration-deficient CX3CR1(-/-) mice the numbers of S. Typhimurium penetrati

231 Cx3cr1(-/-) mice were used to inhibit nonclassical macro

232 argeted key pathways in Ly6C(low) monocytes (Cx3cr1(-/-) mice), Ly6C(high) monocytes (CCR2(-/-) mice)

233 In Cx3cr1(-/-) mice, abGCs exhibited reduced spine density,

234 DSS treatment attenuated disease severity in CX3CR1(-/-) mice, indicating the importance of the micro

235 communication in CX3C receptor-1 deficient (Cx3cr1(-/-)) mice.

236 atory macrophages in liver were increased in Cx3cr1-/- mice, indicating an increased inflammatory res

237 l cord, inflammatory signaling is reduced in CX3CR1(-/-) microglia.

238 pinal cord), the microenvironment created by CX3CR1(-/-) microglia/macrophages enhances NG2 cell resp

239 e of inflammatory stimuli, CX3CR1-deficient (CX3CR1(-/-)) microglia and macrophages adopt a reparativ

240 Interventions that specifically target CX3CR1 might be used in the future to reduce the adverse

241 AC(187)), which is known to block binding to CX3CR1, might decrease disease.

242 (182)CWAIAC(187)), known to block binding to CX3CR1, might decrease disease.

243 and impaired memory formation is mediated by CX3CR1(+) monocyte-derived TNF-alpha.

244 Rather, frequencies of infiltrating CX3CR1(+) monocytes increased over time in livers of Tnf

245 used enhanced infiltration of TH17 cells and CX3CR1(+) monocytes into the injured tissue, which was a

246 d abnormal engraftment of peripheral CCR2(+) CX3CR1(+) monocytes into the retina, which is associated

247 Infiltration of CX3CR1+ monocytes to the peri-infarct zone after MI was

248 Here we show that colonic CX3CR1(+) mononuclear phagocytes are critical inducers o

249 We found that recruited Dock8(-/-)CX3CR1(+) mononuclear phagocytes are exquisitely sensiti

250 esponses mediated by CD11b(+)F4/80(hi)CD64(+)CX3CR1(+) mononuclear phagocytes that contribute to main

251 e-genome microarray screening, we found that Cx3cr1 mRNA levels were substantially higher in microgli

252 ored in neonate mice overexpressing IL-23 in CX3CR1(+) myeloid cells or in keratinocytes.

253 We showed that Cx3cr1(+) and Cx3cr1(neg) i-OCLs differ considerably in transcriptiona

254 Cx3cr1(neg) i-OCLs have a high ability to resorb bone an

255 ated the contribution of mouse Cx3cr1(+) and Cx3cr1(neg) i-OCLs to bone loss.

256 ave in vitro an immune-suppressive effect on Cx3cr1(neg) i-OCLs, mediated by PD-L1.

257 antly lower expression of chemokine receptor CX3CR1 on CD56(bright) NK cells and inhibitory receptor

258 Blocking CX3CR1 or nitric oxide production during G-CSF treatment

259 y to recruit inflammatory Ly6Chi (Ccr2-/- or Cx3cr1-/-) or patrolling Ly6Clo (Ccr5-/-) monocytes.

260 ouse, including established microglial genes CX3CR1, P2RY12 and ITGAM (CD11B).

261 halamic microglial activation via the CX3CL1-CX3CR1 pathway that mediate the resistance of female mic

262 The chemokine receptors CCR2 and CX3CR1 play a major role in monocyte recruitment and dif

263 The G protein-coupled chemokine receptor CX3CR1 plays a central role in several metabolic syndrom

264 effect was associated with lower F4/80- and CX3CR1-positive macrophage infiltration into the liver i

265 rterial macrophages arise embryonically from CX3CR1(+) precursors and postnatally from bone marrow-de

266 Chemokine (C-X3-C) receptor 1 (CX3CR1), predominantly expressed by microglia, suppresse

267 cluding expression of the chemokine receptor CX3CR1, pro-inflammatory cytokines, and granzyme B.

268 Adoptive transfer of Cx3cr1-proficient monocyte-enriched bone marrow cells in

269 numbers of T-regulatory cells and levels of CX3CR1 protein and Il10 mRNA in intestine tissues, and r

270 tal S100-knockout mice had reduced levels of CX3CR1 protein, and Il10 and Tgfb1 mRNAs, compared with

271 The total and cell surface levels of CX3CR1 proteins were also remarkably increased.

272 with expression of the fractalkine receptor CX3CR1 (r2 = 0.99, P = 0.006).

273 Specifically, the activation of the CX3CR1 receptor by fractalkine induces the release of in

274 istically, CX3CL1-mediated engagement of the CX3CR1 receptor induced upregulation of heme-oxygenase-1

275 s little knowledge on how these cells or the CX3CR1 receptor may affect colorectal carcinogenesis.

276 Loss of microglial CX3CR1 receptors, or the specialized extracellular matri

277 whereas plaques transplanted into Ccr2-/- or Cx3cr1-/- recipients lacked this regression signature.

278 ractalkine (CX3CL1), an activating ligand of CX3CR1, regulates organ-specific peritoneal colonization

279 We found that a complete loss of Cx3cr1 restored the responsiveness of Lrrk2(-/-) microgl

280 We show that downregulation of CX3CR1 results in reduction of metastatic burden at seve

281 These CX3CR1(+)SiglecF(+) transitional macrophages localized t

282 at the neuron-to-microglia intercellular FKN/CX3CR1 signaling plays a role in gp120-induced synaptic

283 viously unknown regulatory role for LRRK2 in CX3CR1 signalling and suggest that an increase of CX3CR1

284 odulation of energy homeostasis and identify CX3CR1 signalling as a potential therapeutic target for

285 newed, but also contributed to the expanding CX3CR1(-) Tcm pool.

286 ined by intermediate levels of expression of CX3CR1 that conducts tissue surveillance.

287 high expression of the fractalkine receptor CX3CR1 that has been implicated in endothelial dysfuncti

288 f DC function used markers, such as CD11c or CX3CR1, that are not unique to DCs.

289 Impaired signaling via CX3CR1, the fractalkine receptor, promotes recovery afte

290 pse elimination is dependent on signaling by CX3CR1, the receptor for microglial fractalkine (also kn

291 nds to the corresponding chemokine receptor, CX3CR1, through a CX3C chemokine motif ((182)CWAIC(186))

292 MPhi-tumor cell system, IL-10 drove CCR2 and CX3CR1 up-regulation, whereas CCL1, granulocyte colony-s

293 ying 6 variants associated with MI including CX3CR1 V249I.

294 Higher expression of CX3CL1 and CX3CR1 was confirmed by immunohistochemistry in 100 CRC

295 CX3CR1 was predominantly expressed by macrophages but no

296 e chemokine CX3CL1 and its specific receptor CX3CR1 were significantly upregulated in tumors.

297 Two chemokine receptors, CXCR4 and CX3CR1, were broadly expressed, implying a potentially c

298 d by gp120, and knockout of the FKN receptor CX3CR1, which is predominantly expressed in microglia, p

299 quency, and rare variation in CCR2, CCR5, or CX3CR1 with CAD and MI.

300 Cx3cr1(+) yolk-sac macrophage descendants resided in the