ライフサイエンスコーパス: alternative complement pathway

1 ated with sialic acid, which inactivates the alternative complement pathway.

2 1 inhibitor (C1-INH) as an inhibitor of the alternative complement pathway.

3 rom the bactericidal activity of NHS via the alternative complement pathway.

4 -Ig was more active in inhibiting the murine alternative complement pathway.

5 8 organisms via either the classical or the alternative complement pathway.

6 rabbit erythrocytes due to activation of the alternative complement pathway.

7 ccus neoformans are potent activators of the alternative complement pathway.

8 ulonephritis caused by overactivation of the alternative complement pathway.

9 ent (classical pathway) and amplified by the alternative complement pathway.

10 own how trypanosomes limit the action of the alternative complement pathway.

11 coding variants that directly influence the alternative complement pathway.

12 rulopathies mediated by dysregulation of the alternative complement pathway.

13 posits in patients with dysregulation of the alternative complement pathway.

14 as been associated with dysregulation of the alternative complement pathway.

15 a result, these heparinoids can control the alternative complement pathway.

16 was dependent, in part, on activation of the alternative complement pathway.

17 is caused by uncontrolled stimulation of the alternative complement pathway.

18 ed inhibition of a rate-limiting step in the alternative complement pathway.

19 ent factor H (Cfh) is a key regulator of the alternative complement pathway.

20 vation of C3 to C3b signals the start of the alternative complement pathway.

21 y of tick salivary proteins that inhibit the alternative complement pathway.

22 actor H, a host fluid-phase regulator of the alternative complement pathway.

23 usion (I/R) seems to occur primarily via the alternative complement pathway.

24 veral first-generation drugs that target the alternative complement pathway.

25 binds factor H (fH), a key regulator of the alternative complement pathway.

26 means of evading opsonophagocytosis and the alternative complement pathway.

27 actor B (fB-/-), an essential protein in the alternative complement pathway.

28 human neutrophils but failed to activate the alternative complement pathway.

29 ri comes into contact with components of the alternative complement pathway.

30 ible for the initiation of the activation of alternative complement pathway.

31 to form the pivotal C3-convertase, C3bBb, of alternative complement pathway.

32 an ApoE activated both the classical and the alternative complement pathways.

33 regulates the activity of both classical and alternative complement pathways.

34 eposition on the yeast via the classical and alternative complement pathways.

35 da albicans activates both the classical and alternative complement pathways.

36 affected killing through both classical and alternative complement pathways.

37 yeast and contributions of the classical and alternative complement pathways.

38 tein C, thereby inhibiting the classical and alternative complement pathways.

39 is required to trigger classical as well as alternative complement pathways.

40 iated injury by inhibiting the classical and alternative complement pathways.

41 tes activation of both the classical and the alternative complement pathways.

42 and C4 of the classical and lectin (but not alternative) complement pathways.

43 TNFSF13 locus, 22q12 HORMAD2 locus), and the alternative complement pathway (1q32 CFH/CFHR locus).

44 t factor H (HF1), the major inhibitor of the alternative complement pathway, accumulates within druse

45 The alternative complement pathway (ACP) functions as a surv

46 vating complement proteins to tubular cells, alternative complement pathway activation and C5b-9-medi

47 tablishing that C1q induction and classic or alternative complement pathway activation do not contrib

48 Chronic dysregulation of alternative complement pathway activation has been assoc

49 l classical complement pathway and show that alternative complement pathway activation is an importan

50 ized by transaminitis, thrombocytopenia, and alternative complement pathway activation that peaked on

51 ss the ability to inhibit both classical and alternative complement pathway activation.

52 B autoantibodies as contributing factors in alternative complement pathway activation.

53 ytotoxic antibodies as well as classical and alternative complement pathway activities were determine

54 infections, and led to strong inhibition of alternative complement pathway activity and persistent p

55 essed classical complement pathway activity, alternative complement pathway activity, and the C3 comp

56 ace heparan sulfate (HS) result in increased alternative complement pathway activity, cytolytic damag

57 era from Bf-deficient mice lacked detectable alternative complement pathway activity; purified mouse

58 nd CFHR1, which may themselves influence the alternative complement pathway and are contained within

59 increased gene expression of factor B of the alternative complement pathway and C3 in mouse middle ea

60 sera neutralized virus, suggesting that the alternative complement pathway and complement components

61 s caused by fluid-phase dysregulation of the alternative complement pathway and frequently deviates f

62 ine adipsin/complement factor D controls the alternative complement pathway and generation of complem

63 Factor H (FH) is a critical regulator of the alternative complement pathway and its deficiency or mut

64 soluble CR1 re-establishes regulation of the alternative complement pathway and provide support for a

65 Uncontrolled activation of the alternative complement pathway and secretion of vascular

66 -damaged retina involves the activity of the alternative complement pathway and that eliminating the

67 ury, which was mediated by the classical and alternative complement pathways and reversed by compleme

68 that complement factor H, a regulator of the alternative complement pathway, and LOC387715/HtrA1 are

69 ibe that CC activated both the classical and alternative complement pathways, and C1q was found to be

70 suggests that all-trans-retinal (atRal) and alternative complement pathway (AP) activation contribut

71 The alternative complement pathway (AP) is an important non-

72 Uncontrolled activation of the alternative complement pathway (AP) is thought to be ass

73 The immediate defense provided by the alternative complement pathway (AP) is under constant co

74 s a central role in the amplification of the alternative complement pathway (AP) of the innate immune

75 ingococcal virulence, the molecular basis of alternative complement pathway (AP) regulation by mening

76 The alternative complement pathway (AP) was recently implica

77 vere renal injury secondary to an overactive alternative complement pathway (AP).

78 indings indicate that both the classical and alternative complement pathways are critical for middle

79 HF1), which encodes a major inhibitor of the alternative complement pathway, are associated with the

80 ting factor H (FH), a major regulator of the alternative complement pathway, are associated with vari

81 /ki mice supports systemic inhibition of the alternative complement pathway as a potential treatment

82 d be normalization of activity levels of the alternative complement pathway as measured by C3/C3d rat

83 ides directly and independently activate the alternative complement pathway as well as the classical

84 H, resulting in increased activation of the alternative complement pathway, as a key component of di

85 Human fibroblasts weakly activated the alternative complement pathway, as assessed by C3b depos

86 emonstrated activation of both classical and alternative complement pathways, as indicated by deplete

87 l glomerulosclerosis, cystic kidney disease, alternative complement pathway-associated diseases, or E

88 ntifactor B autoantibodies that activate the alternative complement pathway, bringing self-immunity t

89 A phage Ab against C3b that inhibited the alternative complement pathway, but not the classical pa

90 CC activate the classical and the alternative complement pathways, but the role of the lec

91 ccelerating factor (DAF; CD55), inhibits the alternative complement pathway by accelerating decay of

92 an essential component in suppression of the alternative complement pathway by anti-GXM MAbs.

93 Here, we assessed the role of alternative complement pathway component factor B (FB) i

94 We used alternative complement pathway-deficient (Fb(-/-)) mice

95 -induced retinopathy (OIR), we observed that alternative complement pathway-deficient mice (Fb(-/-))

96 ase-associated CFH genetic variants had more alternative complement pathway deposits than controls.

97 In contrast, blocking of the alternative complement pathway did not protect this uspA

98 rosis (18.0%), cystic kidney disease (9.0%), alternative complement pathway diseases (3.6%), and ESKD

99 Inhibition of the classic but not the alternative complement pathway during reoxygenation atte

100 We investigated the role of the alternative complement pathway during the formation and

101 nabling the bacteria to avoid killing by the alternative complement pathway during vertebrate infecti

102 ANCA-activated neutrophils activate the alternative complement pathway, establishing an inflamma

103 By virtue of its amplifying property, the alternative complement pathway has been implicated in a

104 ormally dampens the activation of C3 via the alternative complement pathway, has been seen in some pa

105 actor that binds a negative regulator of the alternative complement pathway, human factor H (FH).

106 all complement pathways) or CR2-fH (inhibits alternative complement pathway) immediately posttranspla

107 mined the function and key components of the alternative complement pathway in a series of critically

108 fragment (AFD) was generated to inhibit the alternative complement pathway in advanced dry age-relat

109 Results implicate ongoing activation of the alternative complement pathway in AMD pathogenesis.

110 Together, our data implicate the alternative complement pathway in facilitating neovessel

111 The role of the alternative complement pathway in ischemic stroke has no

112 was assayed for its inhibitory effect on the alternative complement pathway in mouse serum.

113 our data suggest a modest involvement of the alternative complement pathway in targeting vessels for

114 wever, little is known about the role of the alternative complement pathway in the initial vascular r

115 antigen processing and presentation, and the alternative complement pathway in the pathogenesis of Ig

116 thy caused by uncontrolled activation of the alternative complement pathway in the setting of autoant

117 Increased activation of the alternative complement pathway in vitreous was controlle

118 was shown to be a selective inhibitor of the alternative complement pathway in vitro and to function

119 e the differential roles of the classical vs alternative complement pathways in EAMG induction, we im

120 cells and shown to inhibit the classical and alternative complement pathways in vitro and in vivo.

121 uman IalphaI inhibited classical, lectin and alternative complement pathways in vitro when added in e

122 ement resistance by recruiting factor H (FH; alternative complement pathway inhibitor) and also by li

123 y treated by inhibiting C4, thus leaving the alternative complement pathway intact.

124 Although the alternative complement pathway is activated in lupus nep

125 Targeting the alternative complement pathway is an attractive therapeu

126 Targeted and selective inhibition of the alternative complement pathway is an effective treatment

127 Candida albicans activates the classical and alternative complement pathways, leading to deposition o

128 tal systems, to be capable of activating the alternative complement pathway, making IgA antibodies po

129 aetiopathogenesis, such as activation of the alternative complement pathway, neutrophil activation vi

130 C1-INH prevented lysis, induced by the alternative complement pathway, of paroxysmal nocturnal

131 AMD patients had increased activation of the alternative complement pathway (P = 0.003) and elevated

132 In a manner that requires activation of the alternative complement pathway, passive transfer of anti

133 Herein we examine recent evidence that the alternative complement pathway plays a key and, in most

134 The alternative complement pathway plays a key role in the p

135 In conclusion, the alternative complement pathway plays a major contributin

136 These data suggest that the alternative complement pathway plays an important role i

137 Since alternative complement pathway recruitment is critical f

138 The alternative complement pathway regulates pathological an

139 H. influenzae strain tested bound factor H (alternative complement pathway regulator).

140 ts within complement factor H (CFH), a major alternative complement pathway regulator, are associated

141 Factor H (fH), a key alternative complement pathway regulator, is a cofactor

142 ies targeting factor H (FH), which is a main alternative complement pathway regulatory protein, have

143 e immune response and that activation of the alternative complement pathway represents one of the inn

144 by blocking C3a complement receptor (C3aR), alternative complement pathway signaling, and antioxidan

145 ere SLE in the absence of both classical and alternative complement pathways suggests that it is the

146 re factor H, a critical downregulator of the alternative complement pathway, than their Por1B counter

147 F-alpha release reflects the activity of the alternative complement pathway that deposits fragments o

148 cterized by fluid-phase dysregulation of the alternative complement pathway that leads to deposition

149 ccount for the spontaneous activation of the alternative complement pathway that occurs after the gen

150 gh factor H is a well known inhibitor of the alternative complement pathway, the functions of the CFH

151 assayed for inhibition of the classical and alternative complement pathways using standard CH(50) an

152 that genetic variation in a regulator of the alternative complement pathway, when combined with a tri

153 ces initiate an inflammatory cascade via the alternative complement pathway, which is unbridled becau

154 disorder characterized by activation of the alternative complement pathway with isolated or dominant