ライフサイエンスコーパス: hepatic macrophage

1 s an EV signature that can retarget EVs from hepatic macrophages.

2 sed Connexin-43 expression in peritoneal and hepatic macrophages.

3 nosyl methionine domain (Rsad2) in liver and hepatic macrophages.

4 e stress activates STING and YAP pathways in hepatic macrophages.

5 altering the transcription and phenotype of hepatic macrophages.

6 egulating inflammatory signaling pathways in hepatic macrophages.

7 s are involved in ALD progression, including hepatic macrophages.

8 eciprocally modulated by ethanol and HA35 in hepatic macrophages.

9 ar proinflammatory phenotypic alterations in hepatic macrophages.

10 r production of osteopontin by NKT cells and hepatic macrophages.

11 he absence of C3a receptor, C5a receptor, or hepatic macrophages.

12 es) in activation of IkappaB kinase (IKK) in hepatic macrophages.

13 ptake and destruction of RBCs by splenic and hepatic macrophages.

14 in monocytes and Kupffer cells, the resident hepatic macrophages.

15 and IFN-alpha/beta produced by LCMV-infected hepatic macrophages.

16 leen and were ingested mainly by splenic and hepatic macrophages.

17 e propensity of hvKp to replicate within the hepatic macrophages.

18 In mice, administration of CSF1-Fc promoted hepatic macrophage accumulation via proliferation of res

19 Furthermore, GW4064 prevented DSS-PN-induced hepatic macrophage accumulation, hepatic expression of g

20 Proinflammatory hepatic macrophage activation plays a key role in the de

21 Treatment of hepatic macrophages after chronic ethanol feeding with s

22 creased ROS associated with CD11b+F4/80+Gr1+ hepatic macrophage aggregation, resulting in transformin

23 trated that prednisolone treatment inhibited hepatic macrophage and neutrophil infiltration in CCl4 -

24 ion analyses, we identified 2 populations of hepatic macrophages and 2 populations of monocytes.

25 ol feeding for 4 days increased apoptosis of hepatic macrophages and activated complement in both wil

26 ressed production of IL1beta and TNFalpha by hepatic macrophages and inhibition of T(H)1/T(H)17 lymph

27 Products of hepatic macrophages and lymphocytes are acknowledged reg

28 ion of classical and alternatively activated hepatic macrophages and natural killer T cells, in the a

29 d the proinflammatory activation of cultured hepatic macrophages and partially blocked liver injury f

30 pendent manner in both adult mouse and human hepatic macrophages and plays an integral role in facili

31 required for iron-induced IKK activation in hepatic macrophages and TAK1, PI3K, and p21ras physicall

32 latory mechanisms and diverse populations of hepatic macrophages and the design of macrophage-targete

33 ated malondialdehyde-LDL (MDA-LDL) uptake by hepatic macrophages and was associated with excess colla

34 main CCR8-expressing cells in the liver were hepatic macrophages, and CCR8 was functionally necessary

35 ensity lipoprotein, increased recruitment of hepatic macrophages, and significant fibrosis.

36 the efflux of recycled iron from splenic and hepatic macrophages, and the release of iron from storag

37 Hepatic macrophages are cellular targets of systemic FXR

38 Circulating monocytes and hepatic macrophages are central mediators of inflammator

39 Our study demonstrates that hepatic macrophages are important in the pathogenesis of

40 Despite the fact that resident hepatic macrophages are known to contribute to early alc

41 Hepatic macrophages are labeled for CSF1R, Mac2 and F4/8

42 acetaminophen-induced injury, with resident hepatic macrophage as the main effector cells.

43 athways of fibrogenesis; (5) re-emergence of hepatic macrophages as determinants of matrix degradatio

44 Hepatic macrophage beta(2) integrin binding to beta-N-ac

45 d no induction of HSC activation pathways by hepatic macrophages but a profound activation of the NF-

46 VDR expression is induced in hepatic macrophages by ER stress, and VDR plays a dual r

47 recognition of mouse and human platelets by hepatic macrophage complement type 3 (CR3) receptors.

48 TM) accumulation is reduced by ~40%, whereas hepatic macrophage content is decreased by ~80%.

49 However, how heterogeneous populations of hepatic macrophages contribute to SCA remains unclear.

50 The level of ISG immunostaining in hepatic macrophages correlated inversely with that of he

51 FoxO1 was upregulated in hepatic macrophages, correlating with hepatic inflammati

52 , lymphocyte antigen 6 complex locus C), and hepatic macrophage cytokine transcription in response to

53 In wild-type hepatic macrophages, deoxycholic acid induced the associ

54 igate origins and epigenetic trajectories of hepatic macrophages during diet-induced non-alcoholic st

55 nd performed an in-depth characterization of hepatic macrophage dynamics and function in models of co

56 y-associated liver disease demonstrates that hepatic macrophage dysfunction occurs in obesity and sug

57 We show for the first time that hepatic macrophages enhance myofibroblast survival in a

58 These observations indicate that splenic and hepatic macrophages export iron during S. Typhimurium in

59 Hepatic macrophages express the highest level of vitamin

60 We show that hepatic macrophages express the primary relaxin receptor

61 pendent outcome of HBV and demonstrated that hepatic macrophages facilitate lymphoid organization and

62 aining liposomes deplete mice of splenic and hepatic macrophages for 5-7 days.

63 Tollip expression was decreased in hepatic macrophages from ethanol-fed rats, but treatment

64 ed HRG is a critical endogenous modulator of hepatic macrophage functionality and investigated its im

65 A marked increase in hepatic macrophages (h-mphi) is observed in experimental

66 ssion in biliary epithelial cells and within hepatic macrophages (h-mpsi) in areas of necrosis.

67 In particular, the critical role of hepatic macrophages has been highlighted and the priming

68 Proinflammatory M1 activation of hepatic macrophages (HM) is critical in pathogenesis of

69 ctivation of M1 phenotypes in isolated mouse hepatic macrophages (HMacs) and in a murine macrophage c

70 it endotoxin-induced NF-kappaB activation in hepatic macrophages (HMs), suggesting a role for the int

71 murine macrophage cell line and rat primary hepatic macrophages (HMs).

72 tellate cells (HSCs), endothelial cells, and hepatic macrophages; however, its role in liver fibrosis

73 or, as well as in wild-type mice depleted of hepatic macrophages; however, there was no increase in h

74 dings underscore the potential importance of hepatic macrophages in regulating both stellate cell bio

75 RNA-sequencing analyses of hepatic macrophages in this model revealed that dietary

76 ts strong anti-inflammatory effects in mouse hepatic macrophages, including those isolated from DIO l

77 ed radiotherapy eliminates immunosuppressive hepatic macrophages, increases hepatic T cell survival a

78 Moreover, VDR deficiency promotes hepatic macrophage infiltration and increases gene expre

79 O treatment determined a strong reduction in hepatic macrophage infiltration and reduced hepatic mRNA

80 nifested further with extramedullary tumors, hepatic macrophage infiltration, and metabolic reprogram

81 f CXCL10 reduced FFC-induced proinflammatory hepatic macrophage infiltration, while natural killer ce

82 y elevated liver ethanol concentrations, and hepatic macrophage infiltration.

83 Specifically, levels of pulmonary and hepatic macrophage inflammatory protein 1alpha (MIP-1alp

84 nduced septic shock, we demonstrate that the hepatic macrophage is the primary source of elevated cir

85 is of SCA, and efficient clearance of VWF by hepatic macrophages is critical for the protective effec

86 TLR4 signaling in hepatic macrophages is increased after chronic ethanol f

87 Depletion of hepatic macrophages led to CD8(+) T cell activation and

88 butions not only of hepatocytes, but also of hepatic macrophages, liver-associated lymphocytes, sinus

89 Hepatic macrophages (MFs) such as Kupffer cells (KCs) ar

90 ia-inducible factors (HIFs) in the liver and hepatic macrophages (MPhis), particularly HIF-2alpha.

91 f posttransplant recipient HO-1 phenotype in hepatic macrophage/neutrophil regulation and function, t

92 ver transplantation reveal increased CD68(+) hepatic macrophage numbers with massive infiltrates of p

93 studies, we analyzed the effects of blocking hepatic macrophages on expression of beta2 integrins and

94 ertheless, depletion of splenic macrophages, hepatic macrophages, or CD4(+) T cells did not affect Gi

95 dels revealed that disease-associated IBA1 + hepatic macrophages originated from bone marrow-derived

96 ulture media of isolated HCs (P < 0.001) and hepatic macrophages (P < 0.001), with HCs being the pred

97 of infiltrating monocytes into cells with a hepatic macrophage phenotype.

98 determined the cellular sources of SLPI and hepatic macrophage phenotype.

99 Although it is well established that hepatic macrophages play a crucial role in the developme

100 ng the composition of the gut microbiota and hepatic macrophage polarization in MASLD mice.

101 tor of transcription 6 (STAT6) signaling and hepatic macrophage polarization that would mediate hepat

102 ds to characterize and analyze sort-purified hepatic macrophage populations that were isolated from m

103 CCR8 critically mediates hepatic macrophage recruitment upon injury, which subseq

104 independent of PAR2 drives CD11b(+)CD11c(+) hepatic macrophage recruitment, and TF-PAR2 signaling co

105 Accordingly, AnxA1 addition to isolated hepatic macrophages reduced galectin-3 expression.

106 Hepatic macrophages (resident tissue KCs and monocyte-de

107 nt of KCs with bone marrow-derived recruited hepatic macrophages (RHMs) that highly express proinflam

108 However, recruited hepatic macrophages (RHMs) were recently shown to repres

109 der lipotoxic conditions, palmitate inhibits hepatic macrophage secretion of IGFBP-3, thereby releasi

110 A sequencing (scRNA-seq) and fate mapping of hepatic macrophage subpopulations, we unraveled the temp

111 artial picture of the full complexity of the hepatic macrophage subsets.

112 s of different inflammatory cells, including hepatic macrophages, T and B lymphocytes, natural killer

113 an age-associated decrease in the numbers of hepatic macrophages that express the scavenger receptor

114 nous hemoglobin increased the sensitivity of hepatic macrophages to subsequent stimulation by LPS.

115 inal injury and IL-1B derived from activated hepatic macrophages to suppress hepatocyte farnesoid X r

116 l injury and IL-1beta derived from activated hepatic macrophages to suppress hepatocyte farnesoid X r

117 The contribution of hepatic macrophages to these events has been largely ove

118 s molecular factor promoting polarization of hepatic macrophages toward the M1 phenotype, thereby pro

119 In homeostatic conditions, hepatic macrophages were overall reduced and preferentia

120 also had a significant increase in F4/80(+) hepatic macrophages, which coexpressed CD11b, suggesting

121 t of CD8(+) T cell responses was mediated by hepatic macrophages, which were predisposed by maternal