ライフサイエンスコーパス: iC3b

1 iC3b contains C3c and thioester domain moieties linked b

2 iC3b deposition on hypoxic (24 hours; 1% O(2))/reoxygena

3 iC3b generation in normal human serum (NHS) was compared

4 iC3b levels were elevated in NHS placed in contact with

5 iC3b was also increased in serum incubated in wells prec

6 site found on the C3c region of iC3b; and 3) iC3b binds to CR2 with different kinetics, depending on

7 4*, and 2.607*; Bb: 0.245, 0.411, and 0.385; iC3b: 10.881, 17.242*, and 15.145*; and SC5b-9: 0.232, 0

8 odel that reconciles conflicting facts about iC3b structure and function and explains the molecular b

9 sites of complement activation by linking an iC3b/C3dg-binding fragment of mouse complement receptor

10 binding domain of complement receptor 3 and iC3b.

11 ocytosis of whole Gram-negative bacteria and iC3b-coated erythrocytes took place only with a full len

12 that Y. enterocolitica YadA recruits C3b and iC3b directly, without the need of an active complement

13 Both C3b and iC3b fragments of C3 bound to S. aureus cells, and about

14 r expressed on macrophages, binds to C3b and iC3b mediating phagocytosis of the particles, but it is

15 Our data predict that C3b and iC3b on opsonized yeast cells direct binding to CR1 and

16 occal cell wall and directly cleaved C3b and iC3b to generate degradation products.

17 ough the kinetics of opsonization by C3b and iC3b was similar for both the CP5(+) and CP8(+) strains.

18 In the present studies, C3b and iC3b were found on several serotype 5 and 8 S. aureus st

19 C3b and iC3b were identified on ECM exposed to purified alternat

20 , resulted in increased affinity for C3b and iC3b, a C3b derivative.

21 f the third component of complement, C3b and iC3b, were bound preferentially by CHO cells transfected

22 f the central complement protein C3, C3b and iC3b, were present on the bacterial surface after incuba

23 RIg, that binds complement fragments C3b and iC3b.

24 amine-cleaved fragments were chiefly C3b and iC3b; 70% of hydroxylamine-sensitive C3b was converted t

25 ure the deposition of C4, factor B, C3b, and iC3b on Staphylococcus aureus.

26 erences exist between the binding of C3d and iC3b to CR2, which may be due to an additional binding s

27 Low levels of circulating C3a, C3d, and iC3b were measured despite the absence of functional cir

28 d the C3 complement fragments C3d, C3dg, and iC3b are essential for the initiation of a normal immune

29 d cytotoxicity and the deposition of C4b and iC3b on the endothelial cells.

30 immune modulating molecule factors H, I, and iC3b.

31 e cell adhesion to ligands such as ICAMs and iC3b.

32 Hyalinous lesions were positive for IgM and iC3b/c/d, indicating subendothelial leakage of plasma pr

33 e the binding sites on both the integrin and iC3b.

34 ng the requirement for CR3 on leukocytes and iC3b on tumors.

35 ugh, of deposited C3b was rapid (<5 min) and iC3b was the dominant fragment on MCP(-) and MCP(+) cell

36 tructure was further validated using an anti-iC3b mAb that was shown to target an epitope in the CUB

37 was shed from the staphylococcal surface as iC3b, regardless of the CP phenotype of the strain.

38 Complement activation products C4d, Bb, iC3b, and SC5b-9 were measured by ELISA.

39 Increases in the plasma levels of C4d, Bb, iC3b, and SC5b-9 were observed in seven of eight patient

40 s study, we analyzed the interaction between iC3b and the 150-kDa headpiece fragment of the CR3 ectod

41 espite high homology, the two integrins bind iC3b at multiple distinct sites.

42 s (K562), and measured their ability to bind iC3b and to conformation-sensitive mAbs.

43 , alphaMbeta2 uses its alphaI domain to bind iC3b at the thioester domain and simultaneously interact

44 Xbeta2 uses the alphaX alphaI domain to bind iC3b on its C3c moiety at one of two sites: a major site

45 The alpha(M) I domain binds iC3b, fibrinogen, intercellular adhesion molecule-1, and

46 or 3 (CR3) directly or through surface-bound iC3b.

47 n of the leukocyte beta2 integrin, CD11b, by iC3b molecules formed from C3 activation in UV-exposed s

48 the more efficient phagocytosis elicited by iC3b than by C3dg and pave the way for the development o

49 ritic cell maturation were also inhibited by iC3b, such as interleukin-12p70 production as well as CD

50 to elicit complement activation, measured by iC3b binding to porcine aortic endothelial cells in vitr

51 that the C3 split products inactivated C3b (iC3b) and C3a were elevated in serum, overlying ARPE-19

52 ntitumor mAb by priming the inactivated C3b (iC3b) receptors (CR3; CD11b/CD18) of circulating granulo

53 in, to an inactive product, inactivated C3b (iC3b), in a step catalyzed by factor I (FI) and its cofa

54 athway toward generation of inactivated C3b (iC3b).

55 y capable of cleaving C3b into inactive C3b (iC3b).

56 A strong staining for C4, C3b, iC3b neoepitope and C9 neoepitope was also found on neur

57 atants were the complement-3 components C3b, iC3b, and C3d, which were upregulated in LTBI and marked

58 increased avidity for the FHR1 ligands C3b, iC3b, and C3dg and enhanced competition with complement

59 aces leads to the massive deposition of C3b, iC3b, and C3dg, the main complement opsonins.

60 e by binding C3 and activation products C3b, iC3b, and C3c, and by blocking the interaction of C5 and

61 HR-1 binds to native C3, in addition to C3b, iC3b, and C3dg.

62 roperdin, bound to a target surface via C3b, iC3b, or other ligands, can use its unoccupied C3b-bindi

63 y cytokines coincided with deposition of C3b-iC3b/C3c (C3b) in the liver.

64 Ethanol-induced deposition of C1q and C3b/iC3b/C3c was colocalized with apoptotic Kupffer cells in

65 y, we characterized the activity of anti-C3b/iC3b monoclonal antibody 3E7 in an in vitro model of APC

66 eactivity assessed with anti-C3 and anti-C3b/iC3b/C3c antibodies, and prevented further spontaneous a

67 ed with the results of factor B binding, C3b/iC3b deposition, and neutrophil association.

68 A panel of complement proteins (C1q, C3, C3b/iC3b, C4, factor B and factor H) were quantified in seru

69 hat complement activation products (C3a, C3b/iC3b) are generated in the serum of experimental mice af

70 significantly higher levels of C4, C4b, C3b/iC3b, CFB, and CFH in the plasma and aqueous humour comp

71 crophage receptor for binding complement C3b/iC3b in vitro, recent studies reveal that CRIg functions

72 loss of PspC also reduced differences in C3b/iC3b deposition between strains.

73 Likewise, C3b/iC3b is more than the opsonizing fragment that facilitat

74 ] ng/mL; controls, 462.5 [132.4] ng/mL), C3b/iC3b, and factor B (MIS-C, 47.6 [7.8] ng/mL; acute COVID

75 Colocalization of C3b/iC3b and CR3 implicated the CR3/iC3b interaction in prim

76 ttack complex (MAC) assembly at sites of C3b/iC3b deposition.

77 ed with SB 290157, and (3) deposition of C3b/iC3b fragments onto the viable bone marrow (BM) cells of

78 was associated with the accumulation of C3b/iC3b/C3c in the liver.

79 te extracellular target) and the opsonin C3b/iC3b (serving as the utility molecule).

80 toxins C3a and C5a as well as opsonizing C3b/iC3b.

81 ation of complement activation products (C3b/iC3b/C3c) in liver and adipose tissue.

82 onal white matter, in close proximity to C3b/iC3b deposits.

83 at FH binding negatively correlated with C3b/iC3b deposition and that median FH binding was high in s

84 the interaction of CR2 with its ligands C3d, iC3b, and the EBV surface glycoprotein gp350/220.

85 tly available mAb is known to block both C3d/iC3b and gp350/220 binding.

86 at serves as the ligand binding site for C3d/iC3b, EBV-gp350, and CD23.

87 these three well-characterized ligands, C3d/iC3b, EBV-gp350, and CD23, a previous study has identifi

88 R2)/CD21 is a B lymphocyte cell membrane C3d/iC3b receptor that plays a central role in the immune re

89 ptor type 2 (CR2/CD21) C3 fragment (C3frag = iC3b, C3dg, C3d)-binding domain with the CAP inhibitory

90 ment activation, resulting in decreased C4b, iC3b, and terminal C5b-9 formation.

91 r D) and activation fragments (Bb, C3a, C5a, iC3b, and SC5b-9) were analyzed.

92 Because in mice, blockade of CD11b (iC3b receptor) on monocytes and depletion of its ligand,

93 by a blocking Ab to CD11b, indicating CD11b-iC3b interaction.

94 e found between BMI and plasma C3, CFB, CFH, iC3b, and C3a.

95 Purified PSA was able to cleave iC3b and the related complement protein C5.

96 nocytes (CD14), TF, and activated complement iC3b and C5b-9 in a human brain thrombus.

97 ns alphaXbeta2 and alphaMbeta2 of complement iC3b-opsonized targets is essential for effector functio

98 ablation of macrophage binding to complement iC3b-coated sheep erythrocytes by MacMARCKS mutant, sugg

99 a2 integrin adhesion to complement component iC3b and ICAM-1 in shear-free, but not shear-flow, condi

100 the thioester domain of complement component iC3b attempting to bind the alpha(M) subunit.

101 ites and interacts with complement component iC3b, agglutinates erythrocytes, and neutralizes influen

102 FACS analysis confirmed iC3b deposition.

103 In contrast, iC3b binding resulted in suppression of IL-12 p40 mRNA a

104 characterized, the nature of additional CR3-iC3b interactions required for phagocytosis of complemen

105 s suggested an affinity of 50 nM for the CR3-iC3b interaction.

106 ation of C3b/iC3b and CR3 implicated the CR3/iC3b interaction in priming.

107 restored by tumor-specific Abs that deposit iC3b onto the tumors.

108 el of glomerulonephritis, the probe detected iC3b/C3d in kidneys of live mice by bioluminescent imagi

109 ined by natural and elicited Abs that direct iC3b deposition onto neoplastic cells, making them targe

110 d a receptor for factor I-cleaved C3b, i.e., iC3b) resulting in the priming of this iC3b receptor for

111 Endothelial iC3b deposition after oxidative stress was also attenuat

112 activated complement fragments, for example, iC3b.

113 Addition of exogenous iC3b, but not C3d, into the DC culture led to the differ

114 lood monocytes entering ultraviolet-exposed, iC3b-containing dermis, purified monocytes from human bl

115 ntly, cell adhesion to the complement factor iC3b is also diminished, and COS cells expressing R77H-s

116 of the ICAM family and the complement factor iC3b.

117 inal helix, which increased the affinity for iC3b approximately 200-fold to 2.4 microM compared with

118 unction and explains the molecular basis for iC3b selective recognition by CR3 on opsonized surfaces.

119 in the eye was monitored by Western blot for iC3b.

120 ed a 30 nM affinity of the CR3 headpiece for iC3b compared with 515 nM for the iC3b thioester domain,

121 beta(2) functions as complement receptor for iC3b and mediates recognition and phagocytosis of pathog

122 oth oral beta-1,3-glucans, a requirement for iC3b on tumors and CR3 on granulocytes was confirmed by

123 complex rationalizes the CR3 selectivity for iC3b.

124 I-domain that contains the binding sites for iC3b, ICAM-1, and fibrinogen.

125 iated cleavage of C3b into the inactive form iC3b and thus prevents formation of inflammatory effecto

126 ated C3 component includes the inactive form iC3b, suggesting that SV5 may have mechanisms to evade t

127 tion-specific protein fragment, C3b, forming iC3b that no longer participates in the complement casca

128 sis, with the complement activation fragment iC3b playing a key effector role.

129 on molecule (ICAM)-1, complement C3 fragment iC3b, and fibronectin, and potently inhibited neutrophil

130 cells opsonized with the complement fragment iC3b and, to a lesser extent, C3dg.

131 t with target-associated complement fragment iC3b, elicit phagocytosis and killing of yeast.

132 e alphaX I domain to the complement fragment iC3b.

133 gands include the complement factor fragment iC3b, a key component in the innate immune defense, whic

134 I domain binding to the complement fragments iC3b and C3d but not to intercellular adhesion molecule-

135 h cannot generate the CR2-binding fragments (iC3b, C3d, and C3dg), were unable to provide costimulato

136 binds to activation-dependent ligands, e.g., iC3b and the mAb 7E3).

137 e to keyhole limpet hemocyanin-coated glass, iC3b-mediated phagocytosis, and homotypic aggregation.

138 aphic structure of the complex between human iC3b and the von Willebrand A inserted domain of the alp

139 e, we then tested the effects of immobilized iC3b and TNF-alpha on resting blood monocytes.

140 B-depleted sera abrogated these increases in iC3b.

141 Several peptides in iC3b showed significantly higher deuterium uptake when c

142 tor I-mediated cleavage of C3b into inactive iC3b.

143 ditions demonstrated significantly increased iC3b deposition in hypoxic/reoxygenated HUVECs compared

144 , yielding CD59-2a-CRIg dimer with increased iC3b/C3b binding avidity and MAC inhibitory activity.

145 xygenation of HUVECs significantly increases iC3b deposition on HUVECs, (2) C3 deposition after hypox

146 Because ultraviolet-induced iC3b deposits are reciprocally maximal on day 3, but fad

147 moted factor I-mediated cleavage of C3b into iC3b as well as decay-accelerating factor (DAF) activity

148 ereas FI-FH proteolytically cleaves C3b into iC3b, PAM-bound hPm catalyzes cleavage of iC3b into mult

149 In this case, FH-FI cleaves C3b into iC3b, with negligible degradation of iC3b by hPm that is

150 or for cleavage and inactivation of C3b into iC3b.

151 ta-1,3-glucan-fluorescein were shown to kill iC3b-opsonized tumor cells following their recruitment t

152 th iC3b and sparing normal tissues that lack iC3b.

153 Therapy fails when tumors lack iC3b, but can be restored by tumor-specific Abs that dep

154 um, they bound less factor I, generated less iC3b on the bacterial surface, and bound fewer C3 fragme

155 ncrease in binding to the physiologic ligand iC3b.

156 18 (alphaMbeta2) with its physiologic ligand iC3b.

157 r) on monocytes and depletion of its ligand, iC3b, reverses UV-induced immunosuppression, we asked wh

158 he avidity of beta2 integrin for its ligand, iC3b, with kinetics similar to those observed in 3H9 mod

159 nt receptor 2 (CR2) with its natural ligands iC3b and C3d are still not well understood.

160 I-less Mac-1 bound to the ligands iC3b and factor X, but this binding was reduced compared

161 D18), as well as to the natural CR3 ligands, iC3b, and Histoplasma capsulatum.

162 on pneumococci than FD(-/-) serum, and more iC3b was deposited onto the PspA(-) than the PspA(+) str

163 3b was generated on the S. aureus surface no iC3b fragments were found, suggesting that other serum p

164 Furthermore, because the ability of iC3b opsonization to enhance phagocytosis of apoptotic c

165 Increased amounts of iC3b were found in trauma sera (n = 27) (vs 12 controls,

166 ted species as the most potent antagonist of iC3b, with a 1.3 microM affinity for the alphaX I domain

167 ion were significantly induced by binding of iC3b in vitro and were synergistically increased by the

168 n, whereas experiments monitoring binding of iC3b to CR3-expressing cells suggested an affinity of 50

169 sociation interface that modulate binding of iC3b with full-length CR2.

170 gion of SCR1 is essential for the binding of iC3b.

171 lization of serum C3 levels and clearance of iC3b from glomerular basement membranes.

172 to iC3b, PAM-bound hPm catalyzes cleavage of iC3b into multiple smaller peptides.

173 alpha1-2 mannobiose, a putative component of iC3b, reported to bind to conglutinin, failed to reveal

174 tes, enabling CR3 to trigger cytotoxicity of iC3b-coated tumors.

175 ng of this iC3b receptor for cytotoxicity of iC3b-opsonized target cells.

176 acrophages, and NK cells for cytotoxicity of iC3b-opsonized tumor cells that otherwise did not trigge

177 3b into iC3b, with negligible degradation of iC3b by hPm that is bound to fibrinogen on the cells.

178 avage to C3b, and accelerated degradation of iC3b by soluble complement receptor 1 (sCR1).

179 Deposition of iC3b and C5b-9 and bacterial killing occurred when bacte

180 F) mobilization results in the deposition of iC3b on BM stroma (stroma-iC3b).

181 work allows us to elucidate determinants of iC3b specificity and activity and provide functional ins

182 ry to describe the structure and dynamics of iC3b at a peptide resolution level in direct comparison

183 ith Cfh(-/-) bone marrow were in the form of iC3b and C3dg, whereas active C3b remained in Cfh(-/-) r

184 proteins, resulting in a predominant form of iC3b that features high structural flexibility.

185 42 was used to investigate the importance of iC3b and CR3 interaction in EAAU.

186 Beta-glucans may also promote killing of iC3b-opsonized tumor cells engendered by administration

187 d state of CR3 that could trigger killing of iC3b-target cells that were otherwise resistant to cytot

188 We explored the kinetics of iC3b opsonization in two models of murine cell apoptosis

189 effects on learned fear were due to loss of iC3b/CR3 signalling.

190 We demonstrate that the C3d moiety of iC3b harbors the binding site for the CR3 alphaI domain,

191 Recognition of iC3b by complement receptor type 3 (CR3) fosters pathoge

192 is immune suppression due to recognition of iC3b opsonized apoptotic cells by CR3, all of the aforem

193 gered because of simultaneous recognition of iC3b via a CD11b I-domain binding site and specific micr

194 otoxic responses require dual recognition of iC3b via the I domain of CD11b and specific microbial su

195 onal binding site found on the C3c region of iC3b; and 3) iC3b binds to CR2 with different kinetics,

196 Furthermore, we show the structure of iC3b in a physiologically-relevant extended conformation

197 er, there is no high-resolution structure of iC3b, and some aspects of its structure-activity profile

198 beta2 and the binding site of alphaMbeta2 on iC3b.

199 hesion, spreading, and migration of cells on iC3b and fibrinogen.

200 Distinctive binding sites on iC3b by integrins alphaXbeta2 and alphaMbeta2 may be bio

201 The integrin-binding sites on iC3b remain incompletely characterized.

202 functions as both a receptor for the opsonic iC3b fragment of C3 triggering phagocytosis or cytotoxic

203 ent receptor (CR1) and an important opsonin (iC3b) are destroyed by proteolytic enzymes.

204 reased binding to the surface-bound opsonins iC3b and C3dg when compared with FH.

205 in which YadA exploits recruitment of C3b or iC3b to attract large amounts of factor H.

206 rted with artificial ligands such as mAbs or iC3b-opsonized RBC.

207 some complement split products, particularly iC3b and C3a; endothelial cells can upregulate various c

208 tion of the complement C3 activation product iC3b to complement receptor type 3 (the iC3b receptor) o

209 essed receptor for the C3 activation product iC3b, implicating C3-CR3 signaling as a regulator of mic

210 ata indicated that C3, its bioactive product iC3b, and the iC3b ligand CD11b are critical for ultravi

211 mplement were used, and the C3 split product iC3b was measured by enzyme immunoassay.

212 enhanced C3 cleavage to activation products iC3b and C3d.

213 assays specific for the activation products iC3b, C4d, Bb, and C5b-9 indicated that ABri and ADan ar

214 d elevation of complement breakdown products iC3b and Ba (P < 0.05).

215 m factor I, a complement regulatory protein, iC3b was generated.

216 expressed on all macrophages and recognizes iC3b on complement-opsonized objects, enabling their pha

217 g R77H-substituted integrins display reduced iC3b-dependent phagocytosis.

218 suggest a critical role for CD55 to regulate iC3b and C5a release and in turn to influence the recrui

219 and assessed whether immobilized and soluble iC3b bound with similar kinetics to CR2.

220 raocular complement activation, specifically iC3b production and engagement of complement receptor 3

221 e present study, we have examined how stroma-iC3b interacts with hematopoietic progenitor cells (HPCs

222 Following irradiation, stroma-iC3b was observed in the presence of purified IgM and no

223 the deposition of iC3b on BM stroma (stroma-iC3b).

224 We demonstrate here that stroma-iC3b tethers HPCs via the inserted (I) domain of HPC com

225 g larger amount of covalently bound C3b than iC3b on the parasite surfaces of MbetaCD-treated promast

226 but fade by day 7, we next hypothesized that iC3b can be responsible for the delay in differentiation

227 We thus hypothesized that iC3b is an important skin-based factor regulating CD11b+

228 cells has been controversial, we report that iC3b opsonization does not significantly affect apoptoti

229 ngle x-ray scattering analysis revealed that iC3b adopts an extended but preferred conformation in so

230 of monocytes for DC maturation revealed that iC3b induced a temporary inhibition of DC differentiatio

231 Immunofluorescence studies revealed that iC3b was newly deposited in UV-exposed skin and was loca

232 lls (IL-3 deprived BaF3 cells), we show that iC3b opsonized apoptotic cells engage CR3, but this inte

233 erived from keratome biopsies suggested that iC3b exposure could inhibit the development of CD1c+ der

234 The iC3b-binding site is located on the MIDAS face and inclu

235 duct iC3b to complement receptor type 3 (the iC3b receptor) on antigen-presenting cells resulted in t

236 that C3, its bioactive product iC3b, and the iC3b ligand CD11b are critical for ultraviolet-induced i

237 Although the interaction between the iC3b thioester domain and the ligand binding CR3 a(M) I-

238 with an anti-CD11b antibody that blocks the iC3b binding site.

239 ration of a fusion protein that contains the iC3b/C3d binding region of complement receptor 2 linked

240 dpiece for iC3b compared with 515 nM for the iC3b thioester domain, whereas experiments monitoring bi

241 In the iC3b fragment, cleavage in an intervening domain creates

242 inant human fusion protein consisting of the iC3b/C3d-binding region of complement receptor 2 (CR2) a

243 s formed between CR3 and regions outside the iC3b thioester domain.

244 rin alpha(X)beta(2) (p150,95) recognizes the iC3b complement fragment and functions as the complement

245 Overall, the data suggest that the iC3b-CR3 interaction is of high affinity and relies on m

246 a, and 3d29) that preferentially bind to the iC3b, C3dg, and C3d fragments in solution, but do not bi

247 a- Glucan had been shown to function via the iC3b-receptor complement receptor 3 (CR3; CD11b/CD18) th

248 In vivo, the iC3b/C3 ratio of SS isolates more closely resembled nons

249 different kinetics, depending on whether the iC3b is in solution or immobilized on the surface.

250 i.e., iC3b) resulting in the priming of this iC3b receptor for cytotoxicity of iC3b-opsonized target

251 e cells did retain the capacity to adhere to iC3b following antibody-induced activation.

252 e or natural killer (NK) cell CR3 adheres to iC3b on erythrocytes or tumor cells that lack CR3-bindin

253 fter sugars blocked primed CR3 attachment to iC3b-targets.

254 Binding to iC3b and factor X by I-less Mac-1 was inhibited by the f

255 HEK293) or constitutive (in K562) binding to iC3b compared with wild-type receptors.

256 Activation of binding to iC3b correlated with exposure of the CBR LFA-1/2 epitope

257 alpha(X)beta(2) is activated for binding to iC3b.

258 When phagocyte CR3 binds to iC3b on bacteria or yeast, phagocytosis and degranulatio

259 did not enhance factor I cleavage of C3b to iC3b and inhibited the cofactor function of factor H.

260 demonstrate that ISG65 stimulates the C3b to iC3b converting activity of complement factor I in the p

261 ion by accelerating the conversion of C3b to iC3b through a unique mechanism.

262 -mediated conversion of surface-bound C3b to iC3b was significantly reduced.

263 proteins may be required for cleaving C3b to iC3b.

264 is liberated during the conversion of C3b to iC3b.

265 , which facilitates the conversion of C3b to iC3b.

266 to bacteria facilitates conversion of C3b to iC3b.

267 I and increased factor I cleavage of C3b to iC3b.

268 These findings suggest that C3b cleavage to iC3b on S. aureus is mediated by serum factor I and does

269 SP, a protease that enhances C3b cleavage to iC3b.

270 C3 binding and almost complete conversion to iC3b on sialylated gonococci.

271 hydroxylamine-sensitive C3b was converted to iC3b within 1 min of opsonization, and the ratio was sta

272 reduction in C3b, which is >75% converted to iC3b.

273 R gonococci, which was promptly converted to iC3b.

274 hese findings suggest that binding of CR2 to iC3b and C3d is more complex than previously thought.

275 e presence of CR1, is cleaved by factor I to iC3b-a and C3c-a and C3dg, all chimeric C3s were cleaved

276 Cleavage of iC3 to iC3b-a by factor I and H was similar in all expressed C3

277 cleavage of deleted (C3delta727-768) iC3 to iC3b-a by factor I in the presence of CR1 was significan

278 C3dg, all chimeric C3s were cleaved only to iC3b-a.

279 istant (SR) gonococci; most was processed to iC3b, yet significant C3b persisted.

280 ence of elevated amounts of C3b processed to iC3b.

281 gonococci but again was processed swiftly to iC3b.

282 in regulates beta(2) integrin avidity toward iC3b by modulating the lateral mobility of beta(2) integ

283 Mo/Mph into an IL-10high/IL-12low state via iC3b in combination with TNF-alpha.

284 eposited in human skin after UV, and whether iC3b can modulate the cytokine profile of Mo/Mph.

285 -induced immunosuppression, we asked whether iC3b is deposited in human skin after UV, and whether iC

286 We investigated whether iC3b opsonized apoptotic cells could induce the same cha

287 Thus, a human skin response in which iC3b is transiently (3-7 d) generated in dermis, such as

288 teraction of cell-bound alpha(M)beta(2) with iC3b, suggesting that it may represent a novel high-affi

289 leukocyte killing of tumor cells coated with iC3b via naturally occurring antitumor antibodies.

290 averages of alpha(X)beta(2) in complex with iC3b define the binding sites on both the integrin and i

291 alphaXbeta2 and alphaMbeta2 in complex with iC3b.

292 Incubation with iC3b markedly inhibited the appearance of CD1c+ cells (p

293 examine the alpha(X)beta(2) interaction with iC3b.

294 e cytotoxicity of tumor cells opsonized with iC3b via anti-tumor Abs.

295 ic tissues that are frequently targeted with iC3b and sparing normal tissues that lack iC3b.

296 In the presence of LPS together with iC3b or fibrinogen, the expression levels of IL-6 and TN

297 and activate complement, coating tumors with iC3b.

298 f alphaMbeta2 ligands (fibrinogen, Factor X, iC3b, ICAM-1 (intercellular adhesion molecule-1), and de

299 icting cleavage to the two sites which yield iC3b through a highly specific catalysis.

300 Cleavage of C3b by fI yields iC3b, a major opsonin.