ライフサイエンスコーパス: complement component

1 omplex with C3d, a fragment of C3, the major complement component.

2 complement but not by serum lacking terminal complement components.

3 hemostasis, has been shown to interact with complement components.

4 absence of, or prior to, expression of other complement components.

5 Higher BMI is related to increased levels of complement components.

6 6 mice or from mice deficient in informative complement components.

7 s soluble pathogen-recognition receptors and complement components.

8 isease dependent upon activation of terminal complement components.

9 gammaIII, complement receptor 2, and various complement components.

10 y of certain coagulation enzymes to activate complement components.

11 utant strains bound similar amounts of early complement components.

12 or C6) mouse sera to differentially deposit complement components.

13 eptors, CR2, binds Ags coated with activated complement components.

14 ic leukemia cells in sera depleted of single complement components.

15 ement pathway, and results in consumption of complement components.

16 r, which has a crucial role in inhibition of complement component 1 (C1) and might implicate the clas

17 teases, C1r and C1s, which reside within the complement Component 1 (C1) complex.

18 arious types of tolerogenic DCs, with ANXA1, Complement component 1 (C1Q), CATC, GILZ, F13A, FKBP5, S

19 Complement component 1 Q subcomponent-binding protein (C

20 latory subunit 2), inflammation (CCL9, CCL6, complement component 1, chitinase3-like 3, TNF superfami

21 1 (Tie-1), collagen type IV alpha1 (Col4a1), complement component 1, q subcomponent receptor 1 (C1qr1

22 Mice with a mutation in complement component 1a (C1qa) were protected from glauc

23 ell function, large deposits of antibody and complement component 1q (C1q) accumulated at sites of ax

24 nohistochemistry with antibodies specific to complement component 1q (C1q).

25 Complement component 1q subcomponent binding protein (C1

26 lta decreases expression of opsonins such as complement component-1qb (C1qb), resulting in impairment

27 ted gene 15 kd], DSP [Desmoplakin], and C1S [complement component 1s subcomplement]) located at three

28 We screened factor B (BF) and complement component 2 (C2) genes, located in the major

29 uirement A serine peptidase 1 (ARMS2/HTRA1), complement component 2 (C2), complement factor B (CFB),

30 studies have identified polymorphisms in the complement component 2 (CC2) and factor B (CFB) genes, a

31 tly, polymorphisms in the factor B (CFB) and complement component 2 (CC2) genes were associated with

32 ed a systematic review of the association of complement component 2(C2)/complement factor B (CFB) gen

33 complement factor H) (P =2.3 x 10(-47)), C2 (complement component 2)-CFB (complement factor B) (P =5.

34 emperature requirement A serine peptidase 1, complement component 2, complement component 3, compleme

35 24), complement component 3 (rs2230199), and complement component 2/complement factor B (rs4151667) w

36 rom complement-mediated damage by inhibiting complement component 3 (C3) activation.

37 single nucleotide polymorphisms (nsSNPs) in complement component 3 (C3) alter the risk of age-relate

38 lobulin binding (Sbi) protein interacts with complement component 3 (C3) and its thioester domain (C3

39 Complement component 3 (C3) deficiency and complement in

40 revealed that the Vi capsule interfered with complement component 3 (C3) deposition.

41 nstead of DCs, which was highly dependent on complement component 3 (C3) from HpSCs.

42 Although complement component 3 (C3) inhibition is known to be va

43 surfaces results in proteolytic cleavage of complement component 3 (C3) into the potent opsonin C3b,

44 We have previously shown that complement component 3 (C3) is secreted by malignant epi

45 Complement component 3 (C3) occupies a central position

46 influences activation of the AMD-associated complement component 3 (C3) promoter fragment and CFB in

47 .03) for neovascular AMD; between T280M and complement component 3 (C3) R102G for AMD (P = .03); bet

48 ncident GA among subjects homozygous for the complement component 3 (C3) R102G rs2230199 nonrisk geno

49 modulated effects we measured, expression of complement component 3 (C3) strongly correlated with cys

50 The complement component 3 (C3) tickover hypothesis was put

51 Complement component 3 (C3) was upregulated in four lept

52 vestigated the molecular mechanisms by which complement component 3 (C3), a central protein in the co

53 component 2 (C2), complement factor B (CFB), complement component 3 (C3), collagen type VIII alpha 1

54 However, the lack of complement component 3 (C3), the predominant complement

55 d a recombinant adenovirus-expressing murine complement component 3 (C3, AdcmvC3).

56 d maculopathy susceptibility 2 (rs10490924), complement component 3 (rs2230199), and complement compo

57 uman CFH protein inhibited cleavage of mouse complement component 3 and factor B in plasma and in ret

58 nvincingly demonstrated to be a receptor for complement component 3 fragments.

59 enhanced uptake was not seen with serum from complement component 3 knockout (C3(-/-)) mice and was a

60 (complement factor B) (P =5.2 x 10(-9)), C3 (complement component 3) (P =2.2 x 10(-3)) and CFI (P =3.

61 serine peptidase 1, complement component 2, complement component 3, complement factor B, collagen ty

62 In contrast, no role of complement component 3, inducible nitric oxide synthetas

63 theless, all three MAbs protected normal and complement component 3-deficient mice from a lethal intr

64 sitive direct antiglobulin tests for IgG and complement component 3; warm autoantibodies were identif

65 n the present study, we examined the role of complement component-3 (C3) using a newly constructed C3

66 mice develop antibodies to this hapten, fix complement component-3 in Bruch's membrane, accumulate d

67 previously reported elevated anaphylatoxins-complement component 3a (C3a) and complement component 5

68 r formation was mediated by EFEMP1(R345W) or complement component 3a (C3a), but not by complement com

69 al lungs, associated with elevated levels of complement component 3a and 5a (C3a and C5a), locally an

70 Targeting the complement component 3a receptor (C3aR) with selective a

71 lidated one of these candidate causal genes, complement component 3a receptor 1 (C3ar1), using a knoc

72 with intravenous immunoglobulin and inactive complement component 3b.

73 rs3818361 single nucleotide polymorphism in complement component (3b/4b) receptor-1 (CR1) is associa

74 1 and ACE were associated with a fragment of complement component 3f.

75 deficient in the classical pathway component complement component 4 (C4) and WT mice pretreated with

76 rom many structurally diverse alleles of the complement component 4 (C4) genes.

77 ity to bind and cleave the effector molecule complement Component 4 (C4).

78 ents positive for the degradation product of complement component 4 (C4d) and acute AMR.

79 unoglobulin M(kappa)] protects wild-type and complement component 4 knockout (C4 KO) mice against let

80 Included are new recommendations for complement component 4d tissue staining and interpretati

81 the genetic absence of C3, thrombin-mediated complement component 5 (C5) convertase activity leads to

82 Complement component 5 (C5) has been described as either

83 We investigated the roles of complement component 5 (C5) in pancreatic fibrogenesis i

84 Using mice genetically deficient in complement component 5 (C5), C6 or the complement regula

85 ceptor-associated factor 1) and C5 (encoding complement component 5).

86 We found a synergistic response to complement component 5a (C5a) in combination with uridin

87 hylatoxins-complement component 3a (C3a) and complement component 5a (C5a)-in IPF, which interact wit

88 generation of the complement anaphylatoxin, complement component 5a (C5a).

89 or complement component 3a (C3a), but not by complement component 5a (C5a).

90 We find that established chemokines, complement component 5a and IL-8 induce chemoattraction

91 e attack complex (MAC)/perforin-like protein complement component 9 (C9) is the major component of th

92 the successful therapeutic application of a complement component, a recombinant form of properdin (P

93 the capacity of anti-HLA antibodies to bind complement components allows accurate risk stratificatio

94 igen-deficient LVS in serum lacking terminal complement components allows efficient uptake of these l

95 complex glomerulonephritis worse, the third complement component also can solubilize immune complexe

96 Complement component C3 is the central complement component and a key inflammatory protein acti

97 tics were calculated to assess the effect of complement components and activation fragments in an AMD

98 ion of cytokine and cytokine receptor genes, complement components and acute phase response genes.

99 esponse genes (IFRGs), antigen presentation, complement components and CD163 antigen were strongly up

100 ole for EGFR in regulating the expression of complement components and complement activation in human

101 Urinary cell levels of mRNA for complement components and complement regulatory proteins

102 R4, and TLR9 induces murine DC production of complement components and local production of the anaphy

103 lization of protein expression for different complement components and regulators were also determine

104 ental factors, including genetic variants in complement components and smoking.

105 with aPL-mediated cell activation, targeting complement components and the innovative concept of bloc

106 y, complement activity and concentrations of complement components and their activation products are

107 ontained small exchangeable apolipoproteins, complement components, and immunoglobulins.

108 IN can recognize C3b in the absence of other complement components, and provide a structural basis fo

109 Mast cells, FcgammaRIII, complement components, and tumor necrosis factor alpha p

110 xogenous source, despite the fact that other complement components are made by KC and upregulated by

111 Polyreactive immunoglobulins (Ig) and complement components are present in tissues and blood o

112 Complete deficiencies of early complement components are strongly associated with syste

113 ly of TLRs, C-type lectin receptors, several complement components, as well as FcepsilonR1.

114 However, the degree and pattern of complement component binding observed suggested that IgM

115 C1q, the recognition subunit of the first complement component, binds to apoptotic cells, thereby

116 evidence for direct activation of individual complement components by extrinsic proteinases as part o

117 lation and activation of alternative pathway complement components by recipient APCs.

118 rations of the complement activation product complement component (C)3a, and immunohistochemical anal

119 ifact to direct blockade of IgG detection by complement component C1 as a possible candidate mechanis

120 Complement component C1, the complex that initiates the

121 , enable completely selective binding to the complement component C1q and activation of complement vi

122 urpose of this study was to evaluate whether complement component C1q binding and activation of the c

123 mical analysis revealed that the increase in complement component C1q is confined to the hippocampal

124 The complement component C1q is known to play a controversia

125 Complement component C1q is required for efficient engul

126 Complement component C1q, beta-chain, nonspecific cytoto

127 recognize and engulf apoptotic cells via the complement component C1q.

128 nteraction with cellular Fc receptors or the complement component C1q.

129 week, including inflammatory markers such as complement components C1q and C2.

130 ated the deposition of gamma heavy chain and complement components C1q and C3 on the surfaces of derm

131 s associated with expression of the upstream complement components C1q and C3, in the absence of memb

132 anscripts are immune related and include the complement components C1q, C3, and C4, which we find are

133 ker (Iba1), a T-lymphocyte marker (CD3), and complement components C1q, C3, factor B, factor H, and m

134 The apparent paradox that early complement component (C1q, C2 and C4) deficiencies predi

135 neuroinflammation including up-regulation of complement component C1QA in microglia/monocytes.

136 nd to eighth thrombospondin-1 motifs and the complement components C1r/C1s, Uegf sea urchin fibropell

137 proconvertase C4b2, followed by cleavage of complement component C2 within C4b2 resulting in the C3

138 of the complex between the d-fragment of the complement component C3 (C3d) and the modular complement

139 We examined the roles of complement component C3 and complement factor B (CFB) in

140 ury to the skin results in activation of the complement component C3 and release of the anaphylatoxin

141 er retina, we examined mice lacking the main complement component C3 and the receptors for complement

142 vivo data indicate that both B cells and the complement component C3 are required for the reduced bac

143 ) both free and bound to the C3c fragment of complement component C3 at 1.5 and 3.4 A resolution, res

144 O antigen prevented both complement component C3 deposition on the surface and co

145 The nature of complement component C3 deposition, i.e., C3b (opsonizat

146 we found that mice deficient in the central complement component C3 displayed increased neovasculari

147 ibody mediated, complement-dependent injury, complement component C3 fragment b (C3b) deposition was

148 Complement component C3 has established roles in both in

149 Autoantibodies against the central complement component C3 have been reported in systemic l

150 ity to restore physiological serum levels of complement component C3 in Cfh KO mice.

151 ing TMEV infection, whereas mice depleted of complement component C3 in the periphery through treatme

152 In the presence of normal serum, complement component C3 is deposited on pneumococci prim

153 Complement component C3 is the central complement compon

154 py demonstrated no significant deposition of complement component C3 on particles.

155 these exoglycosidases reduced deposition of complement component C3 on the pneumococcal surface, pro

156 Complement component C3 plays a particularly versatile r

157 munohistochemistry, and ELISA to examine the complement component C3 split products, C9, VEGF, TGF-be

158 Complement component C3 was found to be an essential ops

159 , mice depleted of PMNs, or mice depleted of complement component C3 were topically treated with MAb

160 C57BL/6 mice, deficient in complement component C3, developed significantly fewer b

161 response genes, MCP-1, STAT1, IL-1beta, and complement component C3, in brain tissue as determined b

162 cient mice showed an enhanced rate of death, complement component C3-deficient mice died even more ra

163 The 1.25-A structure of the complement component C3-inhibitory domain of Staphylococ

164 e most upregulated proteins, followed by the complement component C3.

165 attached, activation-specific, fragments of complement component C3.

166 dent manner from intracellular stores of the complement component C3.

167 decay accelerating factor (DAF), and/or the complement component C3.

168 ing to C3d, a cleavage fragment of the major complement component C3.

169 binding of CR2 to the C3d/C3dg fragments of complement component C3.

170 ial for binding to the target of compstatin, complement component C3.

171 the lung, even in the absence of the central complement component C3.

172 GMVECs were reduced, and gene expression of complement components C3 (C3) and factor B (CFB) was inc

173 The complement components C3 and C1q, but not C5, were requi

174 es for measurement of C1-esterase inhibitor, complement components C3 and C4, and C-reactive protein

175 Among others, we found complement components C3 and C5 in FSAP coimmunoprecipit

176 This study examines the role of complement components C3 and C5 in innate and adaptive p

177 ubretinal pigmented epithelium deposition of complement components C3 and C5 occurs, suggesting a con

178 Mice deficient in complement components C3 and C5 were resistant to the en

179 Deposition of complement components C3 and C5b-9 (the membrane attack

180 lpha showed that Cpa proteolytically cleaved complement components C3, C3a, and C4b.

181 This included complement components C3, C5, C6, apolipoproteins A-I, A

182 Additionally, the deposition of complement components C3, C6, and C5b-9 was enhanced on

183 plasma are rapidly opsonized with the third complement component (C3) via the alternative pathway.

184 une cell infiltrate in mice deficient in key complement components (C3, C5aR), or treated with C5aRa,

185 ic complement assays (AP50, CP50, and LP50), complement components (C3, CFB, CFI, and CFH), and the a

186 Plasma complement components (C3, CFB, CFI, CFH, and factor D)

187 Here, we studied the role of the central complement component, C3, in synaptic health and aging.

188 leavage and activation of the abundant third complement component, C3, via formation of C3-activating

189 inhibits complement activation by binding to complement component, C3.

190 activation-specific fragment of the pivotal complement component, C3.

191 We identify the chemoattractant as the complement component C3a, a factor normally linked with

192 ht to evaluate the pathophysiologic roles of complement components C3a and C5a in the human choroid i

193 e evidence that bioactive fragments of these complement components (C3a and C5a) are present in druse

194 unrecognized in biliary atresia, such as the complement components C3ar-1 and C1q-alpha/beta.

195 is a virulence factor that binds to both the complement component C3b and fibrinogen.

196 irus type 1 (HSV-1) and type 2 (HSV-2) binds complement component C3b and protects virus from complem

197 e complement cascade via an interaction with complement component C3b, we speculate that gCsec could

198 nd a smallpox virus homolog (SPICE) bound to complement component C3b.

199 es as a cofactor for the inactivation of the complement components C3b and C4b, and it also serves as

200 l complement pathways by degrading activated complement components C3b and C4b.

201 The association of complement component C3d with B or T cell complement rec

202 Complement component C4 (C4) is a highly variable comple

203 dividual gene copy-number variation (CNV) of complement component C4 and its associated polymorphisms

204 C1s cleaves complement component C4 and then C2 to cause full activa

205 Complete deficiency of complement component C4 confers strong genetic risk for

206 Complement component C4 is a central protein in the clas

207 C4a is a small protein released from complement component C4 upon activation of the complemen

208 Mice deficient in the downstream complement component C4 were not protected, suggesting t

209 ls of C4d, an activation-derived fragment of complement component C4, are deposited on the surface of

210 identical steps of proteolytic activation of complement component C4, formation of the C3 proconverta

211 demonstrated that coagulation factor IX and complement component C4-binding protein can bind the Ad

212 he HLA codes for the immune effector protein complement component C4.

213 Complement components C4 and C1q were necessary but not

214 The synthesis of complement components C4 and C3 is transcriptionally dow

215 The fourth complement component, C4, and the second component, C2,

216 s have shown that hereditary deficiencies of complement component C4A (a MHC class III gene) confer r

217 Although a heterozygous deficiency of either complement component C4A or C4B is common, and each has

218 resistance of R2866, we compared binding of complement component C4b to R2866 with a serum-sensitive

219 B. burgdorferi, and immunohistochemistry for complement components C4d and C9, CD3, CD79a, and decori

220 za B virus, various bacterial pathogens, and complement components C4d and C9, to identify the cellul

221 omplement-specific drug, an antibody against complement component C5 (eculizumab; Soliris), in March

222 Eculizumab binds complement component C5 and prevents its cleavage by C5

223 In addition, we find that the terminal complement component C5 and the C5a receptor (C5aR) are

224 Complement component C5 binds to components C6 and C7 in

225 We evaluated the role of complement component C5 during the course of cerebral is

226 The role of complement component C5 in asthma remains controversial.

227 (C1) of the classical pathway, activation of complement component C5 via the lectin pathway has not b

228 manized monoclonal antibody directed against complement component C5, eculizumab (Soliris; Alexion Ph

229 VA-induced neutrophil recruitment depends on complement component C5.

230 Although deficiency in the fifth complement component (C5) has been linked to enhanced ai

231 Complement component C5a and ATP are potent effectors of

232 ry protein (MIP)-1alpha, and MIP-1beta], and complement component C5a in bronchoalveolar lavage fluid

233 Inhibiting signaling of the complement component C5a receptor (C5aR) altered the com

234 hil chemotaxis by enzymatically cleaving the complement component C5a.

235 tracheal administration of recombinant mouse complement component (C5a) caused alveolar inflammation

236 Human C8 is one of five complement components (C5b, C6, C7, C8, and C9) that ass

237 promoting CDC in sera depleted of individual complement components C6 to C9.

238 C8alpha, C8beta, and complement components C6, C7, and C9 form the MAC family

239 Complement component C8 plays a pivotal role in the form

240 Complement component C9 immunoprecipitated with the N. f

241 ulates the membrane attack complex (MAC) via complement component C9.

242 ry without the coordinate induction of other complement components, can induce a program of gene expr

243 ctive capture and concentration of activated complement components closer to the cell membrane, poten

244 , it also contains 2 C-terminal CUB domains (complement component Clr/Cls, Uegf, and bone morphogenic

245 ments using human serum depleted of specific complement components demonstrated that the observed lyt

246 we previously demonstrated that the central complement component deposited on the organism's surface

247 Whether NK cells affect complement component expression in HCV-infected hepatocy

248 ratinocytes, EGFR inhibition did not enhance complement component expression or cause complement acti

249 Hepatitis C virus (HCV) proteins inhibit complement component expression, which may attenuate imm

250 pha, yielded a significant downregulation of complement component expression.

251 ration, perivascular deposition of activated complement components, extensive demyelination, loss of

252 We have shown that the complement component ficolin-A significantly binds to As

253 microscopy, monospecific antibodies against complement components, fluorescent secondary antibodies,

254 Soluble complement components form the proteolytic cascade, whos

255 se levels, we documented alternative pathway complement component gene expression within the islets o

256 ines and growth factors and their receptors, complement components, genes associated with cell prolif

257 some neurodegenerative disorders, and active complement components have been detected in the brains o

258 atively regulates beta2 integrin adhesion to complement component iC3b and ICAM-1 in shear-free, but

259 We quantified gene expression of these complement components in cultured human umbilical vein e

260 ssion and differential regulation of several complement components in glaucomatous samples, which inc

261 tion significantly enhanced the induction of complement components in keratinocytes and epidermis fol

262 duction in the levels of Abeta and activated complement components in sub-RPE deposits and structural

263 elease signals that induce the expression of complement components in the CNS.

264 rtance of complement (specifically, terminal complement components) in the pathogenesis of CAPS and t

265 isease course is now identified for multiple complement components (including C1q, C4, and C3) in spi

266 Although the presence of complement components increases after SCI in association

267 the regulation of neovascularization by the complement components is scarce.

268 Searching for other complement components localized at the implantation site

269 KLKs in tissues and biological fluids where complement components may also be expressed, we suggest

270 Because complement components may deposit on RBCs, we asked whet

271 rance of immune complexes, autoreactivity to complement components may have considerable pathological

272 ound proteins accelerate the assembly of the complement components of the alternative pathway on the

273 Albicin also inhibited the deposition of complement components on agarose-coated plates, although

274 signed to define the effects of the terminal complement components on arterial injury in vivo.

275 ed evaluation of the effects of the terminal complement components on graft injury and C4d deposition

276 -activating mAbs efficiently focus activated complement components on the cell, including C3b and C9,

277 D59(-/-) mice with mice deficient in various complement components or receptors including C3, C4, fac

278 Our results show that activated C5 complement components played an important role in cerebr

279 ies provide the first direct indication that complement components produced locally by the RPE are in

280 0 gene (one study, 723 participants) and the complement component receptor 1 gene (one study, 544 par

281 o C3, WT BM cells locally produced all other complement components required to activate C3 and to gen

282 Mice lacking complement components show delayed development of prion

283 In vitro cleavage assays with purified complement components showed that SV5 virions had C3b co

284 nexpectedly, because the disruption of other complement components, such as C1Q, is protective in gla

285 urthermore, ES-62 was shown to deplete early complement components, such as the rate-limiting C4, fol

286 lenged this paradigm by demonstrating that a complement component, the anaphylatoxin C5a, promotes th

287 ortalin can potentially target the C8 and C9 complement components through its ATPase domain and inhi

288 bly of a C3 convertase, which digests the C3 complement component to form microbial binding C3 fragme

289 In this study, we used mice deficient in complement components to investigate the role of complem

290 ers; however, the contribution of individual complement components to lung fibrosis has not yet been

291 yze this reaction assemble from fragments of complement components via multistep reactions.

292 In contrast, the epidermal expression of complement components was downregulated in ex vivo injur

293 However, opsonization of C. gattii with complement components was not sufficient to prolong life

294 found that the epidermal expression of many complement components was only increased to a minor exte

295 Using depleted sera and purified complement components, we demonstrated first that C1q an

296 ed cells reacted with sera depleted of early complement components, we were surprised to discover tha

297 amounts of IgM bound, more of the individual complement components were bound by FX517 than by parent

298 ly in normal or OA ACVs, immunoglobulins and complement components were present only in OA ACVs.

299 ing fibronectin, antimicrobial peptides, and complement components, were associated with S. aureus at

300 rus replication, and increased expression of complement components, which may synergize with vaccine-