ライフサイエンスコーパス: complement activation

1 egulators of the alternative pathway (AP) of complement activation.

2 l impact of FH cleavage on the regulation of complement activation.

3 l link between coagulation, neutrophilia and complement activation.

4 the self from damage inflicted by inadequate complement activation.

5 are consistent with decreased regulation of complement activation.

6 to their surfaces to afford protection from complement activation.

7 igh density to cells and promote substantial complement activation.

8 binding, the first step in classical pathway complement activation.

9 ated neutralization by the lectin pathway of complement activation.

10 and reduced C3b deposition after spontaneous complement activation.

11 heir regulatory function for protection from complement activation.

12 nd the FHR proteins determines the degree of complement activation.

13 e during culture had an inhibitory effect on complement activation.

14 presents a novel mechanism for subversion of complement activation.

15 could contribute to pericyte damage through complement activation.

16 ected reaction monitoring results indicating complement activation.

17 ed that C1q can exert functions unrelated to complement activation.

18 stem and a major fragment produced following complement activation.

19 lement to protect host tissues from aberrant complement activation.

20 with greater intensity and exacerbated local complement activation.

21 g whole-exome sequencing and measurements of complement activation.

22 roteins involved in control of inappropriate complement activation.

23 no effect on C3b cleavage and permit default complement activation.

24 iopulmonary distress in pigs irrespective of complement activation.

25 is enriched with mannan that is resistant to complement activation.

26 ify the severity of myocardial damage due to complement activation.

27 age of complement C3b, thereby shutting down complement activation.

28 s a major role for these proteins regulating complement activation.

29 roteins have an important modulatory role in complement activation.

30 ecular weight enhance the chance of inducing complement activation.

31 pathogen-congregated antibodies and elicits complement activation.

32 rombosis, acute phase response signaling and complement activation.

33 n the bloodstream via mechanisms to suppress complement activation.

34 n inhibitory effect on complement and permit complement activation.

35 ein complexes form in the fluid-phase during complement activation.

36 US) is usually characterized by uncontrolled complement activation.

37 toxicities that may be partially mediated by complement activation.

38 y toward factor I-mediated downregulation of complement activation.

39 ajor regulator of the alternative pathway of complement activation.

40 regulator that protects ECM against damaging complement activation.

41 duce all the proteins required for efficient complement activation.

42 P5 in evasion of the alternative pathway of complement activation.

43 s to the complexity of lectin pathway-driven complement activation.

44 ential enzyme for the lectin pathway (LP) of complement activation.

45 (RPE), is a regulatory protein that inhibits complement activation.

46 hereby inhibiting the alternative pathway of complement activation.

47 hich specifically detects C3d at the site of complement activation.

48 OBZ appear to be annihilated by the lack of complement activation.

49 e is the link between endothelial injury and complement activation.

50 h endothelium perturbation, VWF release, and complement activation.

51 be explained by BCD-mediated attenuation of complement activation.

52 t proteins and the tumor-promoting effect of complement activation.

53 itory therapeutic antibody reversed abnormal complement activation.

54 man leukocyte antigen (HLA) with and without complement activation.

55 ns or autoantibodies leading to dysregulated complement activation.

56 em being possibly due to lack of OBZ-induced complement activation.

57 main regulator of the alternative pathway of complement activation.

58 with markers of disease activity, as well as complement activation.

59 hanistic link between endothelial injury and complement activation.

60 focused on identifying the local triggers of complement activation.

61 eine (SPARC) and collagen-I and induction of complement activation.

62 C3 convertase formation and thereby enhanced complement activation.

63 nd their relatives to (1) test new assays of complement activation, (2) verify whether such abnormali

64 nstrate that LytA has pleiotropic effects on complement activation, a finding which, in combination w

65 dily inducible acute inflammatory responses, complement activation, accelerated cell proliferation an

66 efense mechanism against invading pathogens, complement activation also participates in the adaptive

67 Here we report that astrocytic complement activation also regulates Abeta dynamics in v

68 The complement activation also regulates the efflux and the

69 Complement activation, an integral arm of innate immunit

70 s downregulation of pathways associated with complement activation and acute phase response.

71 Complement activation and binding to beads were revealed

72 g GC-specific IgG autoantibodies, leading to complement activation and C5a generation.

73 nfectious challenge in the colon, leading to complement activation and C5a, which in turn provides pr

74 tor receptor (EGFR) that effectively induces complement activation and CDC, are highly sought after.

75 tivity, inflammatory and calcium signalling, complement activation and cellular response to oxidative

76 lciparum malaria is associated with systemic complement activation and complement-dependent release o

77 ngiopathy characterized by significant serum complement activation and consumption of the complement

78 However, complement activation and function is not confined to th

79 ocalizes to damaged tissue where it leads to complement activation and further tissue damage.

80 Since complement activation and genetic variants in inhibitory

81 sights into the novel modes and locations of complement activation and highlighted unexpected additio

82 rve surfaces, thereby causing injury through complement activation and immune cell recruitment.

83 Our results show that SNPs associated with complement activation and inflammation significantly con

84 ese results highlight links between terminal complement activation and inflammation, endothelial dama

85 Adjusting for the 19 risk SNPs, the complement activation and inflammatory response pathways

86 Complement factor H (FH) inhibits complement activation and interacts with glomerular endo

87 The impact of complement activation and its possible relation to cytok

88 ariants have an impaired ability to regulate complement activation and may benefit more from compleme

89 present an important conceptual advance that complement activation and microglia-mediated synaptic pr

90 we propose a direct mechanistic link between complement activation and neutrophil pHi In this article

91 M1g1 was found to promote complement activation and phagocytosis and protect mice

92 dition of FH5-7 to plasma leads to excessive complement activation and phagocytosis of microbes in fu

93 ogen attachment to host cells and modulating complement activation and phagocytosis.

94 ed for IR-induced mucosal damage, as well as complement activation and proinflammatory cytokine produ

95 ment C3b is crucial for the understanding of complement activation and regulation.

96 interaction, and study the role of FHR-1 in complement activation and regulation.

97 portance of the rate-limiting C4/C2 stage of complement activation and reveal a new addition to the r

98 oth constructs blocked graft IgM binding and complement activation and significantly reduced graft in

99 (RPE), increased oxidative stress, augmented complement activation and slow degeneration of photorece

100 ude that normal plasma VWF multimers prevent complement activation and steer the complement pathway t

101 mechanistically link endothelial damage with complement activation and subsequent TA-TMA.

102 d markers, such as MFGE8 and TREM2, precedes complement activation and synapse loss.

103 progression of fibrosis by attenuating local complement activation and TGF-beta/bone morphologic prot

104 he intricate molecular mechanisms underlying complement activation and the subsequent downstream even

105 portant for H. influenzae resistance against complement activation and will consequently promote bact

106 solid organs is characterized by evidence of complement activation and/or intragraft macrophages (C4d

107 y, MN developed in the absence of detectable complement activation, and disease was strain dependent.

108 celerated antibody-mediated rejection (AMR), complement activation, and graft thrombosis.

109 ent inhibition to sites of tissue injury and complement activation, and in particular to the postisch

110 assical, alternative, and lectin pathways of complement activation, and its cleavage products C3a and

111 cluding type I interferon, interferon gamma, complement activation, and nitric oxide during malaria i

112 MNs showed marked axonal damage after complement activation, and reduced antibody pathogenicit

113 ofuscin accumulation, photooxidative damage, complement activation, and RPE degeneration and may prov

114 in folding, type I interferon production and complement activation, and we further examine their mole

115 joint, which, in combination with classical complement activation, appears to be part of a (patho-)p

116 We investigated whether products of complement activation are capable of providing the primi

117 Drugs that inhibit complement activation are increasingly being used to tre

118 The biological and pathological effects of complement activation are mediated by activation product

119 HDL bound to CC and inhibited the CC-induced complement activation as measured by soluble terminal C5

120 Furthermore, BCD decreased complement activation as measured by terminal complement

121 f 17 candidate genes known to play a role in complement activation as part of a prospective study of

122 ubation of both strains with serum triggered complement activation, as measured by C4b and C3b deposi

123 antibacterial properdin, a regulator of the complement activation, as well as reactive oxygen specie

124 t with age-related neurovascular decline and complement activation, astrocytic Apoe dramatically decr

125 that recruitment of neutrophils triggered by complement activation at the maternal/fetal interface le

126 in de novo lipogenesis, glucose metabolism, complement activation, blood coagulation, and inflammati

127 alternative pathway regulator that controls complement activation both in the fluid phase and on spe

128 RA101295 strongly inhibited E. coli-induced complement activation both in vitro and in vivo by block

129 says have recently been developed to measure complement activation by Abs reactive to specific donor

130 eby we showed that Pic significantly reduces complement activation by all 3 pathways.

131 Although complement activation by bacteria is well documented, wo

132 y active convertases that mediate downstream complement activation by cleavage of C3 and C5.

133 tional analyses indicate that FHR-1 enhances complement activation by competitive inhibition of FH bi

134 The potency of complement activation by IgG Abs can be increased via se

135 functional defects of FH19-20 mutants during complement activation by measuring C3b deposition on mGE

136 Our findings demonstrate that limiting complement activation by neutralizing IL-17A is a potent

137 , these are the first studies to demonstrate complement activation by PF4/heparin complexes, opsoniza

138 terference-specific interventions suppressed complement activation (C3a and C5a) and soluble terminal

139 , ABOiKTx showed a higher rate of intragraft complement activation (C4d deposition) at 5 years compar

140 Eculizumab reduced terminal complement activation (C5a and sC5b-9) and renal injury

141 Complement activation can take place directly on IgA1-co

142 ctive fragments C3a and C5a, produced during complement activation, can modulate both antigen present

143 effector function in primates retain potent complement activation capacity in mice, leading to safet

144 attack complex at the terminal stage of the complement activation cascades via all three activation

145 Patients' T lymphocytes showed increased complement activation causing surface deposition of comp

146 PTX3 deficiency resulted in amplification of Complement activation, CCL2 production, and tumor-promot

147 Although FH systemically controls complement activation, clinical phenotypes selectively m

148 The regulators of complement activation cluster at chromosome 1q32 contain

149 abnormalities from patients with solid-phase complement activation (cluster 4) who had normal or mild

150 analysis separated patients with fluid-phase complement activation (clusters 1-3) who had low serum C

151 in, p < 0.05) and reduced platelet adhesion, complement activation, coagulation activation and inhibi

152 were consistently negative for the terminal complement activation complex C5b9.

153 Complement-activation controllers, including decay accel

154 mals deficient in the C3 protein showed that complement activation could not explain differences in t

155 inhibitors specifically targeted to sites of complement activation, depletion of neutrophils, or bloc

156 they minimize injury in various dysregulated complement-activation disorders, including glomerulopath

157 (the CHAPLE syndrome) is caused by abnormal complement activation due to biallelic loss-of-function

158 L-17A deficiency mitigates bleomycin-induced complement activation during lung fibrosis.

159 Complement activation end products and their receptors m

160 Smoke exposure leads to oxidative stress, complement activation, endoplasmic reticulum (ER) stress

161 athogenesis seems to be the vicious cycle of complement activation, endothelial cell damage, platelet

162 tective CFH haplotype (YY402/II62) showed no complement activation following exposure to either Abca4

163 ll surface in vitro This gain of function in complement activation for two disease-associated CFHR5 m

164 This study investigated the role of the complement activation fragment C5a in secondary patholog

165 es in host defense and homeostasis, with the complement activation fragment iC3b playing a key effect

166 rin to B cells via CD21, and the presence of complement activation fragments on circulating B cells i

167 Complement activation has a major role in thrombotic mic

168 Complement activation has a role in the pathogenesis of

169 n recognized as a model of preeclampsia, and complement activation has been implicated in the high ra

170 In addition, although inappropriate complement activation has long been proposed to cause ti

171 complement protein C5 that inhibits terminal complement activation, has been shown to prevent complic

172 rties, which has been done at the expense of complement activation, has conferred an advantage in som

173 eutrophil serine protease (NSP) activity and complement activation have been implicated in this pheno

174 ed but remained elevated, reflecting ongoing complement activation in aHUS despite complete terminal

175 ectin level of <500 ng/mL) did not influence complement activation in any group.

176 rophage-like cells and lack particle-induced complement activation in autologous human plasma.

177 that such pathology is a function of excess complement activation in Cfh(+/-) mice versus complement

178 analysed and compared different pathways of complement activation in dermatomyositis, lupus nephriti

179 C3d by external body imaging, as a marker of complement activation in heart muscle in a murine model

180 kidney biopsy specimens, but the pathway of complement activation in IMN remains elusive.

181 ies have demonstrated autocrine signaling by complement activation in intracellular vesicles, while t

182 s that we propose to be intimately linked to complement activation in microglia/monocytes.

183 nce complement component expression or cause complement activation in murine keratinocytes.

184 estigate the nature, extent, and location of complement activation in nasal tissue of patients with C

185 the classical pathway plays a major role in complement activation in patients with CRS.

186 classical pathway was a major mechanism for complement activation in patients with CRS.

187 g-based method for non-invasive detection of complement activation in placenta and foetal brain in vi

188 attern recognition molecule that can trigger complement activation in renal epithelial tissue.

189 s been implicated as an important trigger of complement activation in renal tissue.

190 study was to identify molecules that trigger complement activation in rheumatic joints.

191 ability, lack of CD46 leads to dysregulated complement activation in the eye, as evidenced by increa

192 As a result, complement activation in the tumor microenvironment enha

193 that this method may be useful for detecting complement activation in vivo in utero and predicting pl

194 that gigastasin is an effective inhibitor of complement activation in vivo, especially for activation

195 nfusion did not produce measurable levels of complement activation in vivo.

196 ons to OFA did not have markers of increased complement activation in vivo.

197 pneumolysin by a complex process of impaired complement activation, increased binding of complement r

198 mulation of toll-like receptor signaling and complement activation induces expression of proinflammat

199 intramyelinic edema, interleukin-6 release, complement activation, inflammatory cell recruitment, an

200 , antioxidant activity, apoptotic signaling, complement activation, inflammatory response, response t

201 the modified target, FH could prevent excess complement activation initiated by naturally occurring a

202 Complement activation is a recognised mediator of myocar

203 However, complement activation is also peculiarly associated with

204 Complement activation is an important cause of tissue in

205 These include roles in the brain, where complement activation is associated with diseases, inclu

206 Complement activation is normally controlled by regulato

207 The alternative pathway of complement activation is strongly implicated in RPE cell

208 direct link between cholinergic activity and complement activation is supported by in vitro experimen

209 The alternative pathway (AP) of complement activation is the evolutionarily oldest part

210 CD55/DAF, one of the regulators of complement activation, is known to limit excess compleme

211 nset of symptoms, the family history of AMD, complement activation levels (C3d:C3 ratio), the presenc

212 splantation (HSCT) associated with excessive complement activation, likely triggered by endothelial i

213 removed by localized acute immune responses, Complement activation may be prolonged or misdirected to

214 HIV-induced complement activation may contribute to tissue injury du

215 ion and systemic angiopathy and suggest that complement activation may contribute to various human th

216 s provocative study suggests that inhibiting complement activation may heighten immunotherapeutic res

217 Human immunodeficiency virus (HIV)-induced complement activation may play a role in chronic immune

218 t a feedback reaction to cartilage-triggered complement activation observed after a shorter incubatio

219 Marked local and systemic complement activation occurred in GCase-deficient mice o

220 Complement activation occurs during enterohemorrhagic Es

221 st a crucial codominant role of FcRgamma and complement activation of the anti-mLAMalpha3 IgG-induced

222 l-molecule inhibitors of C3 cleavage prevent complement activation on erythrocytes from patients with

223 compete with FH in normal human serum during complement activation on mGEnCs, confirming their potent

224 Complement activation on RBCs could play a role in the h

225 plement regulation by factor H and increased complement activation on renal cell surfaces in vitro an

226 Ab was then used to elucidate the impact of complement activation on the capacity of effector cells

227 Complement activation on the cell surface occurred in co

228 plement activation, is known to limit excess complement activation on the host cell surface by accele

229 l HUS (aHUS), usually caused by uncontrolled complement activation, or as secondary HUS with a coexis

230 ple effector functions such as phagocytosis, complement activation, or neutralization of receptors.

231 Complement activation, oxidative damage, and activation

232 ata suggest that the IgM-H-ficolin -mediated complement activation pathway may be another defensive s

233 population mediated by a novel IgM-H-ficolin complement activation pathway.

234 Of three complement-activation pathways, the alternative and lect

235 identifying a novel relationship between the complement activation peptide C5a and the neural progeni

236 Complement activation plays a major role in many acute a

237 Complement activation plays a vital role in opsonophagoc

238 C5a generated during complement activation possesses proinflammatory and immu

239 The complement activation product C3a is often described as

240 tor and the resulting surface density of the complement activation product C3b, which autoamplifies v

241 Increased levels of the complement activation product C4d, as detected by ELISA

242 These results identify complement activation product C5a as a priming signal fo

243 We measured complement activation products (C3bc and C4bc) and nativ

244 Tissue homogenates were analyzed for complement activation products (ELISA-C5b-9, C4d, activa

245 splantation is mediated through the terminal complement activation products C5a and C5b-9.

246 heumatoid arthritis (RA); elevated levels of complement activation products have been measured in pla

247 olin-3, the associated serine proteases, and complement activation products to CC in vitro using reco

248 bited loss of AQP4 and deposition of IgG and complement activation products, characteristics not seen

249 o, resulting in activation and deposition of complement activation products.

250 We also assessed levels of the complement-activation products C3a, C4a and C5a in these

251 Although there is ample evidence that complement activation provokes overwhelming pro-inflamma

252 Regulators of complement activation (RCA) inhibit complement-induced i

253 fected cells use their surface regulators of complement activation (RCA) to resist antibody-dependent

254 by a family of proteins termed regulators of complement activation (RCA).

255 s, but not lack of Fcalpha/muR expression or complement activation, reduced antiviral IgG responses t

256 Recent work indicates that complement activation regulates key metabolic pathways a

257 This review includes an overview of complement activation, regulatory, and effector mechanis

258 The putative effects of BCD on CC-induced complement activation remain unknown.

259 C3d, a terminal product of complement activation, remains covalently attached to ce

260 classical/lectin and alternative pathways of complement activation, respectively, attenuating the act

261 Lipoproteins can induce complement activation resulting in opsonization and bind

262 ads to a pathogenic level of IgM binding and complement activation, resulting in inflammation and inj

263 d to C4d deposition and to determine whether complement activation results in deposition of the termi

264 Although the other two canonical complement activation routes, the classical and lectin p

265 lation, may be responsible for the increased complement activation seen on the RPE of STGD1 mice.

266 our findings offer functional evidence that complement activation serves as a critical immunomodulat

267 5b-9 membrane attack complex to cells during complement activation shows an inverse correlation betwe

268 tening disease characterized by uncontrolled complement activation, systemic thrombotic microangiopat

269 oteins, CD55 and CD59, leads to uncontrolled complement activation that accounts for hemolysis and ot

270 Our data describe a new trigger mechanism of complement activation that could be important in disease

271 inhibitor (C1-INH) is a soluble regulator of complement activation that negatively regulates the clas

272 In response to complement activation, the membrane attack complex (MAC)

273 ermatomyositis pathology but the trigger for complement activation, the predominant complement pathwa

274 In patients with fluid-phase complement activation, those in clusters 1 and 2 had mas

275 A complete quenching requires complement activation through C3 cleavage and its amplif

276 and alpha- and beta-defensins and regulated complement activation through mannose-binding lectin 2.

277 te C1 and suggests a conserved mechanism for complement activation through the classical and the rela

278 Complement activation triggers a strong inflammatory res

279 Excess complement activation underlies atypical HUS and is evid

280 egulator that promotes the lectin pathway of complement activation via its ability to recruit MBL to

281 A hereditary dysfunction of C3 that prevents complement activation via the alternative pathway (AP) w

282 oke exposure results in oxidative stress and complement activation via the AP, resulting in ER stress

283 FHR-1/CRP interactions increased complement activation via the classical and alternative

284 Initial complement activation via the classical and lectin pathw

285 interfering protein (CIP) that downregulates complement activation via the classical and lectin pathw

286 is strong published evidence indicating that complement activation via the LP critically contributes

287 Complement activation via the terminal pathway is thus i

288 ytes treated solely with the EGFR inhibitor, complement activation was dependent on serum-derived C1q

289 oinflammatory cytokines and EGFR inhibition, complement activation was found even with C1q-depleted s

290 M1g4-mediated complement activation was found to be associated with it

291 Classical complement activation was inhibited by pretreatment of c

292 No complement activation was triggered by cartilage culture

293 induce sub-RPE deposit formation leading to complement activation, which contributes to RPE damage a

294 rstanding of the mechanisms and locations of complement activation, which have added new layers of co

295 t that FHR-1 enhances, rather than inhibits, complement activation, which may explain the protective

296 eneration by recruiting pulp progenitors via complement activation, which suggests to a potential the

297 ced properdin staining correlated with local complement activation with C3b and C5b-9 deposition on t

298 developments indicate that FHRs may enhance complement activation, with important implications for t

299 hrombotic microangiopathy after induction of complement activation within the kidney by accelerated s

300 New methods of detecting complement activation within transplanted organs will im