ライフサイエンスコーパス: CX3CR1

1 acks expression of the fractalkine receptor (CX3CR1).

2 10R, CD206, and CCR2 but little TNF-alpha or CX3CR1.

3 omeruli using beta2 and alpha4 integrins and CX3CR1.

4 is significantly improved in the absence of CX3CR1.

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

6 r macrophages express the chemokine receptor CX3CR1.

7 upon expression of the fractalkine receptor CX3CR1.

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

9 assical monocytes expressed CCR1, CXCR3, and CX3CR1.

10 nds to the corresponding chemokine receptor, CX3CR1.

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

12 set of early T-lineage progenitors expressed CX3CR1, a bona fide marker for DC progenitors.

13 CX3CR1, a cell surface marker whose expression is associ

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

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

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

17 Modulation of CX3CR1 activation in septic mice controlled monocyte adh

18 1 signalling and suggest that an increase of CX3CR1 activity contributes to the attenuated inflammato

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

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

21 Furthermore, the dysfunctional human CX3CR1 allele CX3CR1-M280 was not associated with develo

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

23 er, as to whether common genetic variants in CX3CR1 alter risk of AMD, since prior studies have been

24 L1) with monocyte CX3C chemokine receptor 1 (CX3CR1), although whether ET-1/ETB receptor activation i

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

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

27 Therefore, although CX3CR1 and CX3CL1 act through distinct mechanisms in dif

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

29 ophages were more abundant in the absence of CX3CR1 and produced more of the key profibrotic mediator

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

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

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

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

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

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

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

37 Together, our data suggest that CX3CR1 antagonists and inhibition of FKN proteolytic she

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

39 s, adoptive transfer experiments established CX3CR1 as a key regulator of CD4(+) T cell retention in

40 ted through local proliferation and identify CX3CR1 as a regulator of such proliferation.

41 teatohepatitis progression, which recognizes CX3CR1 as an essential gatekeeper in this scenario.

42 oped a selective, high-affinity inhibitor of CX3CR1 (AZD8797).

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

44 e B(+) cytotoxic cells, which express CD11a, CX3CR1, C-X3-C motif receptor 6 (CXCR6), and CCR10-consi

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

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

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

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

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

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

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

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

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

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

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

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

57 h, the embryo-derived population of resident CX3CR1(+) cMPhi diversifies into MHCII(+) and MHCII(-) c

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

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

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

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

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

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

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

65 Postnatal re-expression of Mecp2 using Cx3cr1(creER) increased the lifespan of otherwise Mecp2-

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

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

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

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

70 CX3CR1 deficiency affected neither antigen presentation

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

72 CX3CR1 deficiency prevents patrolling monocyte migration

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

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

75 ion in APPPS1 animals in a similar manner to CX3CR1 deficiency.

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

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

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

79 not psoriasis, were profoundly decreased in CX3CR1-deficient mice and upon blocking CX3CL1-CX3CR1 in

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

81 l mononuclear phagocytes (MPs) accumulate in Cx3cr1-deficient mice due to the overexpression of APOE,

82 CX3CR1-deficient mice exhibited significantly lower expr

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

84 in light-induced subretinal inflammation of Cx3cr1-deficient mice in vivo.

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

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

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

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

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

90 Cx3cr1-deficient MPs have been shown to increase neurona

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

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

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

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

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

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

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

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

99 Indeed, limiting CX3CR1-dependent signaling could improve rehabilitation

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

101 FP transgenic reporters based upon Csf1r and Cx3cr1 distinguish monocytes from resident mononuclear p

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

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

104 aled that Debio0719 reduced the retention of CX3CR1-EGFP(+) osteoclast precursors in bone by increasi

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

106 mapping demonstrated that cMPhi derived from CX3CR1(+) embryonic progenitors persisted into adulthood

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

108 Furthermore, mice lacking CX3CR1 exhibited a delay in the development of allodynia

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

110 l lamina propria-resident chemokine receptor CX3CR1-expressing macrophages.

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

112 eration in vivo upon skin sensitization, but CX3CR1 expression by both Th2 and Th1 cells was required

113 Lack of Cx3cr1 expression was associated with significantly alte

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

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

116 found negative correlation between CCR2 and CX3CR1 expressions and high-density lipoprotein-choleste

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

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

119 CX3CR1 gene deletion or anti-Abeta immunotherapy causes

120 The CX3CR1 gene is implicated as a candidate gene for age-re

121 ted from APPPS1 mice with the various CX3CL1/CX3CR1 genotypes revealed increased expression of inflam

122 marrow-derived CD68-GFP monocytes to that of CX3CR1(GFP) monocytes in vivo using a sterile zymosan pe

123 Unlike CX3CR1(GFP) monocytes, which downregulate GFP expression

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

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

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

127 Using CX3CR1(GFP/+)CCR2(RFP/+) reporter mice, we show that TBI

128 Exposure of Cx3Cr1(gfp/Delta)Abca4(-/-)Rdh8(-/-) mice to intense lig

129 iminished APOE and CCL2 levels and protected Cx3cr1(GFP/GFP) mice against harmful subretinal MP accum

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

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

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

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

134 of APOE-dependent subretinal inflammation in Cx3cr1(GFP/GFP) mice, the APOE4 allele led to diminished

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

136 rmful subretinal MP accumulation observed in Cx3cr1(GFP/GFP)TRE3 mice.

137 261-induced mouse models in combination with CX3CR1(GFP/WT);CCR2(RFP/WT) double knock-in mice.

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

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

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

141 ssed CD206, whereas tissue-derived AAMs were CX3CR1-GFP and CD206 negative.

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

143 Monocyte-derived AAMs were also CX3CR1-green fluorescent protein (GFP)(high) and express

144 X3CL1 (fractalkine) and its unique receptor, CX3CR1, have been observed in human AD.

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

146 man DCs-MPhis and anti-inflammatory CD11c(+) CX3CR1(hi) cells isolated from murine gut tissue.

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

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

149 ing agent in the colon and define intestinal CX3CR1(hi) macrophages as a decisive factor that determi

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

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

152 In this manner, CX3CR1(hi) patrolling monocytes serve as immune-privileg

153 emokine, MCK2, which promotes recruitment of CX3CR1(hi) patrolling monocytes to initial infection sit

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 3(hi) and localize to lung parenchyma or are CX3CR1(hi)KLRG1(hi) and are retained within lung blood v

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

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

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

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

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 ons, these findings would support a role for CX3CR1 in AMD but also suggest that its role may involve

170 of the chemokine receptors CCR5, CXCR3, and CX3CR1 in classical monocytes were higher in HTLV-1-infe

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

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

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

174 etween the ET-1/ETB receptor axis and CX3CL1/CX3CR1 in mediating pulmonary angiogenesis and vascular

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

176 The role of CX3CR1 in MS and EAE pathogenesis however remains to be

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

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

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

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

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

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

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

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

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

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

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

188 CX3CR1(int) Tmem cells underwent more frequent homeostat

189 3CR1-deficient mice and upon blocking CX3CL1-CX3CR1 interactions in wild-type mice.

190 CXCL16 was constitutively expressed by CX3CR1(+) intestinal dendritic cells (DCs) and coexpress

191 CX3CR1 is a chemokine receptor involved in leukocyte adh

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

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

194 ation of the innate immune responses through CX3CR1 is crucial for controlling steatohepatitis progre

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

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

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

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

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

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

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

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

203 ency of the microglial fractalkine receptor (CX3CR1) led to the acceleration of tau pathology and mem

204 sed viremia) expressed lower CCR2 and higher CX3CR1 levels than monocytes from HIV-negative controls.

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

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

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

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

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

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

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

212 tive (Ki67(+)) Lin(-)c-Kit(+)CD135(-)CD115(+)CX3CR1(+)Ly6C(+)CD11b(-) subpopulation, consistent with

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

214 rmore, the dysfunctional human CX3CR1 allele CX3CR1-M280 was not associated with development of recur

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

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

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

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

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

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

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

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

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

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

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

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

227 on of fluorescence-labeled CD4+ T cells into Cx3CR1 mice (mice exhibiting GFP-labeled HSCs) after I/R

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

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

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

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

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

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

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

235 AngII/Cx3cr1(-/-) mice, however, significantly increased macro

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

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

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

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

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

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

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

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

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

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

246 resulting in the infiltration of circulating CX3CR1(+) monocytes into the sciatic nerve.

247 At the endothelial-nerve interface, CX3CR1(+) monocytes were activated by the chemokine CX3C

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

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

250 and IL-1beta inhibition efficiently blunted Cx3cr1-MP-dependent photoreceptor apoptosis in a monocyt

251 Here, we demonstrate CX3CR1 mRNA expression on inflammatory cells within acti

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

253 CX3CR1 neutralizing antibody partially inhibited ET-1 ef

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

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

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

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

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

259 Depletion of CX3CR1(+) phagocytes was assessed in mice by live-cell c

260 CD3 or antigen caused transient depletion of CX3CR1(+) phagocytes, which was prolonged by co-injectio

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

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

263 cells (DC) expressing the chemokine receptor CX3CR1 populates most tissues.

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

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

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

267 1 of which, rs2853707, is positioned in the CX3CR1 promoter region and was associated with neovascul

268 diet and methionine/choline-deficient diet), CX3CR1 protected mice from excessive hepatic steatosis a

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

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

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

272 Notably, deficiency for the microglial CX3CR1 receptor has opposing effects on Abeta and MAPT p

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

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

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

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

277 unlike in allergic asthma, where CX3CL1 and CX3CR1 regulate the pathology by controlling effector CD

278 We recently reported that CX3CR1 regulates the abundance of CD11c(+) DC in the kid

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

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

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

282 T-1/ETB receptor activation modulates CX3CL1/CX3CR1 signaling and lung angiogenesis in experimental H

283 k between MPhi and cancer cells via CCR2 and CX3CR1 signaling as a central underlying mechanism.

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

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

286 1, the neuronally derived cognate ligand for CX3CR1, signals both in membrane-anchored and soluble fo

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

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

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

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

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

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

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

294 ying 6 variants associated with MI including CX3CR1 V249I.

295 e modes of association and that an effect of CX3CR1 variants may depend on other factors including di

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

297 CX3CR1 was predominantly expressed by macrophages but no

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

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

300 ltration of peripheral leukocytes expressing CX3CR1 would be a suitable treatment strategy for MS, we