ライフサイエンスコーパス: anaphylatoxin

1 ting to the pro-inflammatory response to the anaphylatoxin.

2 , histamine, platelet activating factor, and anaphylatoxin.

3 ctivation products, including the potent C3a anaphylatoxin.

4 rom respiratory failure that was ascribed to anaphylatoxins.

5 tion of proinflammatory products such as the anaphylatoxins.

6 g factor, leukotriene B4, and the complement anaphylatoxins.

7 ng of pathogens and the production of potent anaphylatoxins.

8 revents cold agglutinin-driven generation of anaphylatoxins.

9 ent manner generating functional C3a and C5a anaphylatoxins.

10 , can directly generate bioactive complement anaphylatoxins.

11 ht polyanions increased degradation of these anaphylatoxins.

12 ase activity leads to the generation of C5a (anaphylatoxin), a promoter of vasodilatation and permeab

13 C5a anaphylatoxin, a potent inflammatory mediator, is known

14 The C5a anaphylatoxin acting on its cognate G protein-coupled re

15 , indicating that G-proteins are involved in anaphylatoxin-activated signal transduction pathways.

16 rscoring its role as a negative regulator of anaphylatoxin activity.

17 These complement anaphylatoxins also could be generated by beta-tryptase

18 cells, suggesting a cross-influence between anaphylatoxin and chemokine axes.

19 ed the underlying mechanism(s) of complement anaphylatoxin and chemokine cooperation.

20 sults in significantly reduced formations of anaphylatoxins and membrane-attack complexes.

21 ses suggested a physical association between anaphylatoxins and the constant region of F(ab)2.

22 importance of complement activation, the C3a anaphylatoxin, and its receptor during Th2 development i

23 ly induced complement deposition, release of anaphylatoxins, and CDC against distinct tumor cell line

24 C3a and C5a anaphylatoxins are cytokine-like polypeptides generated

25 vated levels of beta-tryptase and complement anaphylatoxins are detected.

26 The anaphylatoxins are potent, complement-derived low m.w. p

27 e regulated by allergen-driven production of anaphylatoxins, as mouse strains deficient in complement

28 omplement activator that directs chemotactic anaphylatoxin C3a and C5a production, was induced 34-fol

29 The complement anaphylatoxin C3a and its cellular seven-transmembrane s

30 e that both lipopolysaccharide (LPS) and the anaphylatoxin C3a are needed for IL-1beta production in

31 The anaphylatoxin C3a has been reported to have immunomodula

32 ects, we assessed the role of the complement anaphylatoxin C3a in a mouse model of pulmonary allergy

33 The anaphylatoxin C3a is a potent chemotactic peptide and in

34 The anaphylatoxin C3a is released from C3 during complement

35 lin resistance, and loss of signaling by the anaphylatoxin C3a prevents obesity-induced insulin resis

36 Previous studies suggest that the anaphylatoxin C3a promotes, whereas C5a protects from th

37 topoietic progenitors express the complement anaphylatoxin C3a receptor (C3aR) and respond to C3a.

38 In this study, we investigated the anaphylatoxin C3a receptor (C3aR) in Chlamydia psittaci

39 The anaphylatoxin C3a receptor (C3aR) is unique among the fa

40 HNFAG09 encodes the human anaphylatoxin C3a receptor.

41 Treatment of human macrophages with anaphylatoxin C3a results in stimulation of C3 transcrip

42 ssion of complement C3 and production of the anaphylatoxin C3a, and down-regulates the expression of

43 The complement anaphylatoxin C3a, on binding the C3aR, mediates numerou

44 -induced degranulation, but had no effect on anaphylatoxin C3a-induced response.

45 e complement component C3 and release of the anaphylatoxin C3a.

46 lting in various cleavage products including anaphylatoxin C3a.

47 induce complement activation, producing the anaphylatoxin C3a.

48 absolutely no interaction of C5L2 with other anaphylatoxins C3a and C4a.

49 Mast cells express receptors for complement anaphylatoxins C3a and C5a (ie, C3a receptor [C3aR] and

50 The anaphylatoxins C3a and C5a are liberated as activation b

51 model, we have demonstrated that complement anaphylatoxins C3a and C5a are required for the survival

52 investigators have implicated the complement anaphylatoxins C3a and C5a as potential effectors in Typ

53 tiple C3 and C5 cleavage fragments including anaphylatoxins C3a and C5a as well as opsonizing C3b/iC3

54 These results suggest that the anaphylatoxins C3a and C5a present in injured tissues co

55 The comparative ability of the complement anaphylatoxins C3a and C5a to mediate leukocyte adhesion

56 mbrane attack complex formation, but not the anaphylatoxins C3a and C5a, activated the NLRP3 inflamma

57 gnals, including substance P, the complement anaphylatoxins C3a and C5a, and endothelin 1, induced hu

58 al similarity between C4a and well-described anaphylatoxins C3a and C5a, the binding partner and biol

59 exogenous immunoglobulin molecules also bind anaphylatoxins C3a and C5a, thereby neutralizing their p

60 alternative pathway led to generation of the anaphylatoxins C3a and C5a, which recruited neutrophils

61 phlogistic molecules, such as the complement anaphylatoxins C3a and C5a.

62 The complement anaphylatoxins C3a, C5a, and desarginated C5a (C5a(desAr

63 l, lectin, or alternative pathways generates anaphylatoxins (C3a and C5a) and membrane attack complex

64 suggested the involvement of the complement anaphylatoxins (C3a and C5a) in the development of aller

65 for assays of mast cell tryptase, histamine, anaphylatoxins (C3a, C4a, C5a), cytokines (IL-2, IL-6, I

66 plement system with subsequent generation of anaphylatoxins (C3a, C5a) and the terminal complement co

67 The complement anaphylatoxins, C3a and C5a, exert their effects by bind

68 Growing evidence suggests that anaphylatoxins, C3a and C5a, play important roles in inn

69 omplement protein C3 or the receptor for the anaphylatoxin C5a (C5aR) from Daf-1(-/-) mice reversed t

70 termined whether there are receptors for the anaphylatoxin C5a (C5aR, CD88) on human mesangial cells

71 C5 activation that blocks generation of the anaphylatoxin C5a and C5b, an essential component of MAC

72 The complement anaphylatoxin C5a and its seven-transmembrane segment (7

73 ents the 3D model of the complex between the anaphylatoxin C5a and its specific receptor, C5aR.

74 C5aR is a G protein-coupled receptor for the anaphylatoxin C5a and mediates many proinflammatory reac

75 ly inhibited neutrophil migration toward the anaphylatoxin C5a and suppressed neutrophil-dependent in

76 local C5 concentration and production of the anaphylatoxin C5a and the cytolytic C5b-9 complex.

77 mase, also express CD88 and are activated by anaphylatoxin C5a and the secretagogue compound 48/80.

78 pHi These data suggest a novel role for the anaphylatoxin C5a as a master switch of the delicate pHi

79 nd indicate that, after binding to C5aR, the anaphylatoxin C5a causes significant up-regulation of ce

80 The anaphylatoxin C5a constitutes a powerful fragment genera

81 ion of a critical C-terminal arginine of the anaphylatoxin C5a disabled the protein function.

82 rophils treated with the chemoattractant and anaphylatoxin C5a exhibited a prolonged activation (>15

83 The complement anaphylatoxin C5a functions through its two receptors, C

84 The anaphylatoxin C5a has been implicated in the pathogenesi

85 The anaphylatoxin C5a impairs phagocytosis by neutrophils.

86 We also assessed the levels of anaphylatoxin C5a in the cerebrospinal fluid of patients

87 The complement anaphylatoxin C5a is a critical mediator of allergic con

88 Anaphylatoxin C5a is a potent inflammatory mediator asso

89 The anaphylatoxin C5a is a potent mediator of inflammation t

90 The complement anaphylatoxin C5a is a proinflammatory component of host

91 e previously reported that generation of the anaphylatoxin C5a is linked to the development of cardia

92 y previously unknown mechanisms by which the anaphylatoxin C5a limits acute inflammation and antagoni

93 e model of breast cancer that the complement anaphylatoxin C5a receptor (C5aR) facilitates metastasis

94 The complement anaphylatoxin C5a receptor (C5aR) has been implicated in

95 the complement system with generation of the anaphylatoxin C5a results in profound disturbances in cr

96 rimental sepsis, excessive generation of the anaphylatoxin C5a results in reduction of the C5a recept

97 Anaphylatoxin C5a was a potent chemotaxin (EC50 approxim

98 cells (HBECs) toward the complement-derived anaphylatoxin C5a when these cells are exposed to cigare

99 our study on the production and role of the anaphylatoxin C5a, a potent immune mediator generated af

100 another complement activation fragment, the anaphylatoxin C5a, and Fcgamma receptors (FcgammaRs) bee

101 asma-based systems, measuring release of the anaphylatoxin C5a, and generation of C5b, the initial co

102 ocyte chemotactic protein 3 (MCP-3), and the anaphylatoxin C5a, induce activation, degranulation, che

103 monstrating that a complement component, the anaphylatoxin C5a, promotes the growth of malignant tumo

104 ttraumatic immune response is the complement anaphylatoxin C5a, which acts via two receptors, C5aR1 a

105 ment activation and generation of the potent anaphylatoxin C5a.

106 icans infection was largely dependent on the anaphylatoxin C5a.

107 ement components and local production of the anaphylatoxin C5a.

108 The complement anaphylatoxins C5a and C3a are released at the inflammat

109 ed from the chemokine, complement fragment 5 anaphylatoxin (C5a), can act as agonists or antagonists

110 Complement C5A anaphylatoxin (C5A), lipopolysaccharide binding protein

111 The complement-derived anaphylatoxin, C5a, is a potent phlogistic molecule that

112 In response to the anaphylatoxin, C5a, or to PMA treatment, IL-16 mRNA tran

113 , CX3C chemokine receptor 1 (CX3CR1), or C5a anaphylatoxin chemotactic receptor (C5aR).

114 we also demonstrate that GelE can cleave the anaphylatoxin complement C5a and that this proteolysis l

115 sfunction after generation of the complement anaphylatoxin, complement component 5a (C5a).

116 Whereas we have previously reported elevated anaphylatoxins-complement component 3a (C3a) and complem

117 lator of the biologic activity of kinins and anaphylatoxins, CPN is an important regulator of the bio

118 CS induced generation of C3a and C5a, potent anaphylatoxins derived from complement proteins.

119 ctivation, and a final product, in which the anaphylatoxin domain has undergone a remarkable movement

120 C3 is converted to C3b by proteolysis of its anaphylatoxin domain, by either of two C3 convertases.

121 To better understand the roles of C anaphylatoxins during inflammation, we investigated thei

122 the C3 cleavage product C3a, a member of the anaphylatoxin family.

123 This anaphylatoxin functions by interacting with two 7-transm

124 C3a, C4a, and C5a anaphylatoxins generated during complement activation pl

125 activation of FSAP by tissue injury triggers anaphylatoxin generation and thereby modulates the postt

126 Anaphylatoxin generation was measured by ELISA, Western

127 he complement system, the stable form of C3a anaphylatoxin (ie, C3a-desArg).

128 C5a is the most potent of the three anaphylatoxins in eliciting biological responses.

129 , we analyzed the role of complement-derived anaphylatoxins in the pathogenesis of experimental acute

130 gest beta-tryptase might generate complement anaphylatoxins in vivo at sites of inflammation, such as

131 re consistent with the actions of complement anaphylatoxins, in particular C3a and C5a.

132 emonstrate that locally produced C5a and C3a anaphylatoxins interacting with their G protein-coupled

133 logically active peptides such as complement anaphylatoxins, kinins, and fibrinopeptides.

134 s a modular glycoprotein with amino-terminal anaphylatoxin-like modules followed by nine epidermal gr

135 istry analysis of lung tissue indicated that anaphylatoxins may regulate airway hyperresponsiveness (

136 Furthermore, we discuss the control of anaphylatoxin-mediated activation of dendritic cells and

137 ing the early phase of reperfusion, and both anaphylatoxin-mediated inflammation and the membrane att

138 ue injury following stroke and suggest a C3a anaphylatoxin-mediated mechanism.

139 ite role in regulating the lethal effects of anaphylatoxin-mediated shock, 2) that these lethal effec

140 We show here that the complement-derived C5a anaphylatoxin negatively regulates TLR4- and CD40-induce

141 It is now well appreciated that anaphylatoxins not only act as pro-inflammatory mediator

142 We highlight the influence of anaphylatoxins on Th2 and Th17 cell development during a

143 in through the release and action of the C5a anaphylatoxin peptide.

144 The presence of the complement-derived anaphylatoxin peptides, C3a and C5a, in the lung can ind

145 l and alternative pathways of complement and anaphylatoxin production (reflected in significant rises

146 tibodies and complement, upstream complement anaphylatoxin production exacerbates endothelial exocyto

147 eactions are strongly believed to arise from anaphylatoxin production through complement activation.

148 The C3a anaphylatoxin receptor (C3aR) is a G protein-coupled rec

149 The C5a anaphylatoxin receptor (C5aR; CD88) is activated as part

150 moting function of the Galpha(i)-coupled C5a anaphylatoxin receptor by liver macrophages in vivo.

151 d chemotaxis but not macrophage CCR2 and C5a anaphylatoxin receptor expression were reduced in the sp

152 in human disease, yet little is known about anaphylatoxin receptor gene regulation.

153 ype mice, indicating that neither complement anaphylatoxin receptor is critical for ECM development.

154 nique role for C5L2 in negatively modulating anaphylatoxin receptor mediated cellular activation thro

155 ted that gene-targeted disruption of the C5a anaphylatoxin receptor prevented lung injury in immune c

156 athway (AP) of complement and complement C3a anaphylatoxin receptor signaling were analyzed using kno

157 (i2) and Galpha(i3), including mediating C5a anaphylatoxin receptor-induced activation of macrophages

158 ingly, actin rearrangement and CCL2- and C5a anaphylatoxin receptor-induced chemotaxis but not macrop

159 complex injury, as did disruption of the C5a anaphylatoxin receptor.

160 t such effects are directly mediated through anaphylatoxin-receptor signaling in cDCs.

161 eptors in a related family that includes the anaphylatoxin receptors and the formyl-MetLeuPhe recepto

162 okine production in vivo was mediated by the anaphylatoxin receptors C5aR and C3aR.

163 d to function similarly to those of mammals, anaphylatoxin receptors have not previously been charact

164 that the response was mediated by the known anaphylatoxin receptors in a G(i) activation-dependent f

165 Signaling of anaphylatoxin receptors or assembly of membrane attack c

166 HUVEC constitutively expressed both anaphylatoxin receptors, and addition of physiological c

167 Contribution of the anaphylatoxin receptors, C3aR and C5aR, to the pathogene

168 Whereas C4a showed no activity toward known anaphylatoxin receptors, it acted as an agonist for both

169 erum levels of sFlt1 correlated with C5a, an anaphylatoxin released after complement activation.

170 The test stimulus for these studies was anaphylatoxin split product of C component (C5a), which

171 regeneration through the local production of anaphylatoxins such as C5a.

172 Moreover, blockade of anaphylatoxins, such as C5a, offers a promising approach

173 Complement factor 5a (C5a) is an anaphylatoxin that acts by binding to a G protein-couple

174 ned presence of IFN-gamma and C5-derived C5a anaphylatoxin that was deficient among these macrophages

175 ts indicate a unique function for complement anaphylatoxins that implicate these molecules in the ind

176 Signaling of the C3a anaphylatoxin through its G protein-coupled receptor, C3

177 while additionally generating C5a and other anaphylatoxins, to which pulmonary xenografts may be uni

178 try verified that the molecular mass of each anaphylatoxin was correct.

179 ttranslational modification pattern of these anaphylatoxins, which includes glycosylation at Asn(64)

180 ced cytokines in favor of complement-derived anaphylatoxins, which then guide the cells toward nearby

181 ally biased decapeptide agonist of human C5a anaphylatoxin (YSFKPMPLaR) was used as a molecular adjuv

182 ally biased decapeptide agonist of human C5a anaphylatoxin (YSFKPMPLaR) was used as a molecular adjuv