ライフサイエンスコーパス: complement activation

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

2 heir regulatory function for protection from complement activation.

3 iopulmonary distress in pigs irrespective of complement activation.

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

5 roteins have an important modulatory role in complement activation.

6 rombosis, acute phase response signaling and complement activation.

7 hereby inhibiting the alternative pathway of complement activation.

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

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

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

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

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

13 itory therapeutic antibody reversed abnormal complement activation.

14 ck ligand binding by local CL-11 and prevent complement activation.

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

16 ns or autoantibodies leading to dysregulated complement activation.

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

18 main regulator of the alternative pathway of complement activation.

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

20 hanistic link between endothelial injury and complement activation.

21 focused on identifying the local triggers of complement activation.

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

23 C3 convertase formation and thereby enhanced complement activation.

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

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

26 l link between coagulation, neutrophilia and complement activation.

27 the self from damage inflicted by inadequate complement activation.

28 are consistent with decreased regulation of complement activation.

29 to their surfaces to afford protection from complement activation.

30 igh density to cells and promote substantial complement activation.

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

32 ated neutralization by the lectin pathway of complement activation.

33 and reduced C3b deposition after spontaneous complement activation.

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

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

36 presents a novel mechanism for subversion of complement activation.

37 could contribute to pericyte damage through complement activation.

38 ected reaction monitoring results indicating complement activation.

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

40 stem and a major fragment produced following complement activation.

41 o acid levels were associated with increased complement activation.

42 must therefore rely on inhibitors to counter complement activation.

43 nts are present in cSCC biopsies, indicating complement activation.

44 ohistochemistry, and associated with in situ complement activation.

45 r Factor H, resulting in the deregulation of complement activation.

46 MDA-modified surfaces, resulting in enhanced complement activation.

47 icantly correlated with disease severity and complement activation.

48 is limited infarct size, but did not prevent complement activation.

49 release as the temperature-limiting step in complement activation.

50 ge of DAF from podocyte surfaces, leading to complement activation.

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

52 Complement activation alone was necessary and sufficient

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

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

55 The complement activation also regulates the efflux and the

56 Complement activation, an integral arm of innate immunit

57 hich may due to IgG immune complex triggered complement activation, anaphylatoxin and cytokine releas

58 e as a "second hit," leading to uncontrolled complement activation and a more severe thrombotic pheno

59 Despite evidence of complement activation and a robust T cell response, the

60 11 or collectin kidney 1 (CL-K1)), initiates complement activation and acute kidney injury.

61 At this l-fucose dose, complement activation and acute post-ischemic kidney inj

62 in both the classical and lectin pathways of complement activation and also inhibits the contact, coa

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

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

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

66 ification in an unexpected crosstalk between complement activation and coagulation signaling.

67 excretion but also leads to ammonia-induced complement activation and deposition of C3 and C5b-9 tha

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

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

70 Since complement activation and genetic variants in inhibitory

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

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

73 l cycle gene (RGCC), a gene that responds to complement activation and induces apoptosis in endotheli

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

75 ease COVID-19 patients, we describe systemic complement activation and its association with developme

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

77 -dependent neutrophil/monocyte phagocytosis, complement activation and natural killer cell activation

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

79 parasite Plasmodium berghei triggers robust complement activation and ookinete elimination upon mosq

80 In reperfused and non-reperfused stroke, complement activation and opsonization of hippocampal sy

81 r both reperfused and non-reperfused stroke, complement activation and opsonization of hippocampal sy

82 munoglobulin molecules are needed to trigger complement activation and opsonization.

83 ur pilot study points towards aberrations in complement activation and oxidative damage in IPF patien

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

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

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

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

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

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

90 Moreover, the complement activation and the procoagulant effects of th

91 hat the lectin pathway likely contributed to complement activation and tissue injury in this strain.

92 estore original target binding, to eliminate complement activation and to improve protein stability.

93 rget of antiphospholipid Abs responsible for complement activation and vascular thrombosis in patient

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

95 e corona proteins involved in lipid binding, complement activation, and coagulation.

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

97 Renal function and histology, complement activation, and expression of kidney injury m

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

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

100 The copolymer complexes show no complement activation, and in vivo lung tolerance studie

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

102 he heart proteome included vasoconstriction, complement activation, and lipoprotein metabolism enrich

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

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

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

106 sotype profile, Fc-gamma receptor usage, and complement activation are all intertwined factors that s

107 the mechanisms regulating the efficiency of complement activation are poorly understood.

108 tablishes immunoglobulin-driven dysregulated complement activation as a critical pathobiological mech

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

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

111 y subjects, to monitor nanoparticle-mediated complement activation as well as C3 opsonization.

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

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

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

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

116 monstrate that ERp57 can negatively regulate complement activation, but also identify a control mecha

117 toward engineering of nanosurfaces with low complement activation, but due to promiscuity of complem

118 Greater complement activation by 2C7-E430G Fc translated to incr

119 not by a factor D inhibitor, indicating that complement activation by anti-beta2GPI antibodies occurs

120 Although complement activation by bacteria is well documented, wo

121 tivating potential and that ERp57 suppresses complement activation by cleaving disulfide bonds in fic

122 attenuated ficolin-3 ligand recognition and complement activation by cleaving intermolecular disulfi

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

124 r level, MCs act as potent effector cells of complement activation by expressing receptors for C3a an

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

126 ntation of antibody binding, and blockade of complement activation by inhibitors expressed on target

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

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

129 tin triggered an unconventional mechanism of complement activation by noncovalent anchoring of C3 act

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

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

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

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

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

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

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

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

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

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

140 es (e.g., ABA, circulating immune complexes, complement activation, complete blood counts, cytokine/c

141 Complement-activation controllers, including decay accel

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

143 history of macular degeneration (a proxy for complement-activation disorders) and history of coagulat

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

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

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

147 This reveals a novel mechanism of complement activation during streptococcal sepsis, which

148 Complement activation end products and their receptors m

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

150 y processes for asthma pathogenesis, such as complement activation, extracellular matrix organization

151 an blood and plasma revealed no hemolysis or complement activation following incubation with these si

152 We highlight the importance of complement activation for antigonococcal Ab function in

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

154 d that biliverdin inhibits the expression of complement activation fragment 5a receptor one (C5aR1) i

155 The complement activation fragment C5a is a potent proinflam

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

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

158 flammation revealed widespread deposition of complement-activation fragments throughout the sinusoids

159 Complement activation generates the core effector protei

160 Complement activation has been implicated as contributin

161 Uncontrolled complement activation has been implicated in several hum

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

163 llowing surface-target binding and increases complement activation (HexaBody technology) showed signi

164 In response to antibody-mediated complement activation, IFN-gamma-primed human ECs intern

165 trospective study investigated mechanisms of complement activation in 34 children with acute postinfe

166 Our results suggest a pivotal role for complement activation in BD-induced renal injury and pos

167 entified thrombin as a surrogate pathway for complement activation in C3-deficient mice.

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

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

170 ides a framework for understanding classical complement activation in human autoantibody-mediated dis

171 ains) of human CD55 on nanoparticle-mediated complement activation in human sera and plasma.

172 didates for preventing nanomedicine-mediated complement activation in human subjects.

173 tection in C3-deficient mice and evidence of complement activation in humans have led to the hypothes

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

175 , specifically, apoptotic cell clearance and complement activation in kidney disease development.

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

177 in allergic asthma and the lectin pathway of complement activation in nonallergic asthma.

178 tic effect of severe ADAMTS13 deficiency and complement activation in pathogenesis of TMA in mice.

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

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

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

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

183 C5b-9 in vitro but does not prevent upstream complement activation in response to SARS-CoV-2 spike pr

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

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

186 ndicate that CFH is critical for controlling complement activation in the liver, and in its absence,

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

188 patients with severe COVID-19 show prominent complement activation in their lung, skin, and sera, and

189 HuCR1 and compared their ability to inhibit complement activation in vitro using multiple assays.

190 COVID-19 serum induced complement activation in vitro, consistent with high com

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

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

193 ctions, increased markers of coagulation and complement activation (including tissue factor and C5a),

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

195 LRP3-independent mechanisms, and (3) whether complement activation induces inflammasome activation in

196 ed by an accumulation of proteins related to complement activation, inflammation and modulation of im

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

198 Complement activation is a recognised mediator of myocar

199 However, complement activation is also peculiarly associated with

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

201 Systemic complement activation is associated with respiratory fai

202 osition of C5b-9 to test the hypothesis that complement activation is associated with thrombotic even

203 h circulating parasites and antibody-induced complement activation is indispensable for CRIg-mediated

204 Complement activation is normally controlled by regulato

205 However, aberrant complement activation is often observed in autoimmune di

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

207 Thus, complement activation is tightly regulated by a series o

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

209 cally-relevant radiotherapy induces aberrant complement activation, leading to brain injury.

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

211 Systemic complement activation levels are increased during pregna

212 tabolites were associated significantly with complement activation levels, independent of AMD status.

213 the AMD-associated metabolites and systemic complement activation levels, independent of AMD status.

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

215 highly enriched for connected genes in early complement activation linked to measures of disease seve

216 strates, components of the lectin pathway of complement activation: mannose-binding lectin, ficolin-2

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

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

219 Inhibition of complement activation may have multiple beneficial effec

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

221 Clinical reports have suggested that complement activation may play a role in the development

222 Subjects with higher complement activation measured by elevated blood sC5b-9

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

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

225 Complement activation occurs during enterohemorrhagic Es

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

227 We also detected in vivo classical complement activation on CD4+ T cells in 14% of the whol

228 IRI induces immunoglobulin M-dependent complement activation on endothelial cells that assemble

229 quired to the platelet surface, resulting in complement activation on M1-activated human platelets.

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

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

232 Complement activation on the cell surface occurred in co

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

234 Developmental failure was caused by complement activation on trophoblasts in Cmas-/- implant

235 is, platelet activation and aggregation, and complement activation or coagulation were analyzed.

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

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

238 Components from the complement activation pathway were predominantly increas

239 and cell death in excitatory neurons via the complement activation pathway.

240 universal and is observed regardless of the complement activation pathway.

241 LXR/RXR activation and complement activation pathways were enriched in t-test s

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

243 biologically potent molecules, including the complement activation peptides, C3a and C5a.

244 neutrophil and macrophage infiltration, and complement activation (plasma C5a) and deposition (tissu

245 Complement activation plays a vital role in opsonophagoc

246 Complement activation plays an important role in pharmac

247 ata indicate that donor-management targeting complement activation prevents the development of DGF.

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

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

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

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

252 Complement activation products covering the classical/le

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

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

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

256 ated gain-of-function change (D1115N) to the complement-activation protein C3 results in aHUS.

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

258 such as RA, deposited ApoE may induce local complement activation rather than exert its typical role

259 which primarily belong to the regulators of complement activation (RCA) family.

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

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

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

263 to Doxil treatment suppresses Doxil-induced complement activation-related pseudoallergy (CARPA) in p

264 LSPD was well tolerated, and no complement activation-related pseudoallergy reactions we

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

266 ng mechanisms of the pathognomonic transient complement activation, remains uncertain.

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

268 Complement activation results in clearance of pathogens,

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

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

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

272 maturation, we found that IgA deposition and complement activation significantly increased and led to

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

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

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

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

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

278 -19 the subsequent endothelial inflammation, complement activation, thrombin generation, platelet, an

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

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

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

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

283 Initial complement activation via the classical and lectin pathw

284 ern recognition molecules that contribute to complement activation via the lectin pathway.

285 Complement activation via the terminal pathway is thus i

286 HLA class I expression, and posttransfusion complement activation was increased in clinical TRALI.

287 Classical complement activation was inhibited by pretreatment of c

288 Plasma heme and complement activation was markedly increased in one pati

289 Consistently increased systemic complement activation was observed in the majority of CO

290 ulating immune complex levels increased, and complement activation was observed.

291 No complement activation was triggered by cartilage culture

292 s in plasma and eyecup lipoproteins, but not complement activation, which correlated with the AMD-lik

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

294 ab, a monoclonal antibody, inhibits terminal complement activation, which impairs the ability of the

295 ted KCNH2-3.1 potassium channel in mediating complement activation, which may explain its association

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

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

298 his nanobody may be valuable for analysis of complement activation within animal models of both acute

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

300 own regarding the role of CFH in controlling complement activation within the liver.