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 tion via elaboration of complement-dependent anaphylatoxins.

5 , can directly generate bioactive complement anaphylatoxins.

6 ht polyanions increased degradation of these anaphylatoxins.

7 rom respiratory failure that was ascribed to anaphylatoxins.

8 tion of proinflammatory products such as the anaphylatoxins.

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

10 ng of pathogens and the production of potent anaphylatoxins.

11 revents cold agglutinin-driven generation of anaphylatoxins.

12 ent manner generating functional C3a and C5a anaphylatoxins.

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

14 C5a anaphylatoxin, a potent inflammatory mediator, is known

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

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

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

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

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

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

21 une complex triggered complement activation, anaphylatoxin and cytokine release, etc., leading to acu

22 the complement derived effectors, opsonins, anaphylatoxins and membrane attack complex (MAC), have b

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

24 inct binding pocket topologies of complement anaphylatoxins and provide key insights into receptor ac

25 at IL-1beta induces expression of complement anaphylatoxins and suppresses the complement-inactivator

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

27 y preventing the generation of C5a, a potent anaphylatoxin, and C5b, the first step in the eventual f

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

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

30 and C5 directly in tubular fluid, generating anaphylatoxins, and that this is attenuated by amiloride

31 C3a and C5a anaphylatoxins are cytokine-like polypeptides generated

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

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

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

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

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

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

38 The anaphylatoxin C3a has been reported to have immunomodula

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

40 The anaphylatoxin C3a is a potent chemotactic peptide and in

41 The anaphylatoxin C3a is released from C3 during complement

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

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

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

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

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

47 ion of the C3a and C5a receptors (complement anaphylatoxin C3a receptor [C3aR] and complement anaphyl

48 HNFAG09 encodes the human anaphylatoxin C3a receptor.

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

50 The antiapoptotic signaling downstream of anaphylatoxin C3a signaling in tumor cells contributed t

51 quent maturation complement C3 maturation to anaphylatoxin C3a was dependent on PCa epithelial inhibi

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

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

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

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

56 lting in various cleavage products including anaphylatoxin C3a.

57 induce complement activation, producing the anaphylatoxin C3a.

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

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

60 The anaphylatoxins C3a and C5a are liberated as activation b

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

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

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

64 combination of uPA and plasminogen generated anaphylatoxins C3a and C5a from intact C3 and C5 and was

65 e nephrectomy, we tested the hypothesis that anaphylatoxins C3a and C5a in donor urine before transpl

66 In particular, the anaphylatoxins C3a and C5a played an important role in t

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

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

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

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

71 , and the terminal products of this cascade, anaphylatoxins C3a and C5a, exert their physiological an

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

73 tor molecules of the complement cascade: the anaphylatoxins C3a and C5a, the opsonins C4b and C3b, an

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

75 itates feeding by blocking production of the anaphylatoxins C3a and C5a, which activate mast cells le

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

96 The anaphylatoxin C5a constitutes a powerful fragment genera

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

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

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

100 The anaphylatoxin C5a has been implicated in the pathogenesi

101 The anaphylatoxin C5a impairs phagocytosis by neutrophils.

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

103 The anaphylatoxin C5a is a complement peptide associated wit

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

105 Anaphylatoxin C5a is a potent inflammatory mediator asso

106 The anaphylatoxin C5a is a potent mediator of inflammation t

107 The complement anaphylatoxin C5a is a proinflammatory component of host

108 The anaphylatoxin C5a is core effector of complement activat

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

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

111 d complement inhibitors to determine whether anaphylatoxin C5a mediates VOE.

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

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

114 hylatoxin C3a receptor [C3aR] and complement anaphylatoxin C5a receptor 1 [C5aR1]) on human umbilical

115 l activation and synaptic loss, elevation of anaphylatoxin C5a receptor, astrocytic-C3, and microglia

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

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

118 Anaphylatoxin C5a was a potent chemotaxin (EC50 approxim

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

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

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

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

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

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

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

126 Here, we identified the complement anaphylatoxin C5a-mediated activation of C5a receptor 1

127 ement components and local production of the anaphylatoxin C5a.

128 ment activation and generation of the potent anaphylatoxin C5a.

129 icans infection was largely dependent on the anaphylatoxin C5a.

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

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

132 Complement C5A anaphylatoxin (C5A), lipopolysaccharide binding protein

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

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

135 sits and restore RPE epithelial phenotype in anaphylatoxin challenged iPSC-RPE with or without the CF

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

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

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

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

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

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

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

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

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

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

146 This anaphylatoxin functions by interacting with two 7-transm

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

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

149 Anaphylatoxin generation was measured by ELISA, Western

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

151 emoattraction and activation are mediated by anaphylatoxins in a paracrine and autocrine fashion.

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

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

154 ions with proteinuria, uPA-plasmin generates anaphylatoxins in tubular fluid and promotes downstream

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

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

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

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

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

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

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

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

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

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

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

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

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

168 IgE or their receptors, by molecules such as anaphylatoxins, or through G-coupled receptors.

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

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

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

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

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

174 C5a is an anaphylatoxin protein produced by the cleavage of the co

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

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

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

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

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

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

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

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

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

184 tudy, we have examined the role of the third anaphylatoxin receptor, C5aR2, in the host immune respon

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

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

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

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

189 ucidates the innerworkings of the complement anaphylatoxin receptors and should facilitate structure-

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

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

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

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

194 Signaling of anaphylatoxin receptors or assembly of membrane attack c

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

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

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

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

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

200 ceRI) by allergens or Ags and the binding of anaphylatoxins such as C3a to its receptor, C3aR.

201 onRI) by allergens or Ags and the binding of anaphylatoxins such as C3a to its receptor, C3aR.

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

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

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

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

206 ascade, leading to exaggerated production of anaphylatoxins that are responsible for neutrophil recru

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

208 ment cascade, resulting in the production of anaphylatoxins that sustain tumour-promoting inflammatio

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

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

211 is dependent on AMD-risk-allele CFH(H/H) and anaphylatoxin triggered alternate complement signaling v

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

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

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

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

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