ライフサイエンスコーパス: IgG3

1 red by the presence of LTP-specific IgG1 and IgG3.

2 ered the production of IFN-gamma, IgG2a, and IgG3.

3 nd the IgG exclusively consisted of IgG1 and IgG3.

4 plasma cells and reduced levels of IgG2b and IgG3.

5 s were each paired with human IgG1, IgG2, or IgG3.

6 ount for near-normal levels of serum IgM and IgG3.

7 th up to 50-fold increases in serum IgG1 and IgG3.

8 showed higher levels of anti-MDA-LDL IgM and IgG3.

9 t and with production of anti-LIMS1 IgG2 and IgG3.

10 P), and the role of anti-envelope (anti-Env) IgG3.

11 reases in all subtypes with the exception of IgG3.

12 ns of all Ig isotypes were low, particularly IgG3.

13 ndent on FcgammaRIII, with IgG1>IgG2b>>IgG2a=IgG3.

14 -1 and MSP-1(42) were predominantly IgG1 and IgG3.

15 -1(neg) B-1 cells are also a major source of IgG3.

16 The IgG3-1 subclass switch interacts with B cell-receptor af

17 Anti-CD28-PV1-IgG3, a hamster-mouse chimeric antibody against murine C

18 IgG3 Ab of females but not males also correlated with de

19 hematopoietic cells had intermediate IgM and IgG3 Ab responses after NP-Ficoll immunization, suggesti

20 odestly increased in NOS2(-/-) mice, IgM and IgG3 Ab responses as well as marginal zone B cell plasma

21 ificantly higher alpha-gal-specific IgG1 and IgG3 Ab than nonallergic individuals, whereas the latter

22 ated (active) LPS boosted polyclonal IgM and IgG3 Ab titers.

23 vated levels of Env-specific IgG1, IgG2, and IgG3 Abs compared with males.

24 Both IgG1 and IgG3 Abs demonstrated similar EGFR binding and similar e

25 gp140-specific IgG3 Abs of females but not males were correlated with A

26 Env-specific IgG and IgG3 Abs, IgG avidity, and neutralizing Abs inversely co

27 cells to produce complement-fixing IgG1 and IgG3 Abs.

28 polymorphism and transplacental transfer of IgG3, adjusting for hypergammaglobulinemia, maternal mal

29 , we demonstrate that an optimal response to IgG3-Ag complexes requires that CR1/2 is expressed on bo

30 a suggest that CR1/2(+) MZ B cells transport IgG3-Ag-C complexes from the MZ to the follicles, where

31 studies of IgG subclass responses identified IgG3 against a peptide derived from MSP3 as the stronges

32 prevalent in LN serum, which also contained IgG3 against the antigen panel and anti-C1q IgG4.

33 other with low-to-moderate-affinity IgG1 and IgG3 also later developed low-titer FVIII inhibitors.

34 Together, these data suggest human anti-EGFR-IgG3, although highly reactive with C1q, to weakly promo

35 protection against malaria and further shows IgG3 and GLURP antibodies are key in the OP mechanism, t

36 switch slightly better to IgG2a, IgG2b, and IgG3 and have more S region DSBs and mutations than wild

37 a fusion protein consisting of anti-HER2/neu-IgG3 and IFN-alpha (anti-HER2/neu-IgG3-IFN-alpha) and in

38 but displayed significantly lower levels of IgG3 and IFN-gamma compared with adults.

39 IgE, IgG1, IgG3 and IgA1 transcripts showed reduced somatic hypermu

40 fectively elicits class-switched NP-specific IgG3 and IgG2b in mice.

41 nover rate during activation of switching to IgG3 and IgG2b, as well as delays in CSR kinetics associ

42 ariants showed protection in vitro, with the IgG3 and IgG4 variants showing the highest protection in

43 quence with those of other subclasses (IgG2, IgG3 and IgG4) showed that these aggregation-prone motif

44 estingly, the F240 isotype-switched variants IgG3 and IgG4, also expressed in CHO cells, exhibited id

45 IgG and IgG1-4 by ELISA, anti-HLA-total IgG, IgG3 and IgG4, and donor-specific antibody by Luminex as

46 ased significantly, and heavy depositions of IgG3 and IgM were observed in intervillous spaces.

47 nt Ags displayed elevated T cell-independent IgG3 and T cell-dependent IgG2b responses.

48 s were moderately stronger for IgG1 than for IgG3 and were ineffective for Fab.

49 40, mostly low-to-moderate-affinity IgG1 and IgG3, and 1 had high-affinity IgG4 and later developed l

50 ically significant enrichment of fibrinogen, IgG3, and complement components, especially C1q.

51 uced glomerular accumulation of IgG1, IgG2a, IgG3, and complement, while low-dose DMPA decreased glom

52 splacental transport with wild-type IgG1 and IgG3, and found transport across trophoblast-derived BeW

53 uced titers of secreted class-switched IgG1, IgG3, and IgA antibodies, without alterations in critica

54 Natural Abs, belonging to isotypes IgM, IgG3, and IgA, were discovered nearly half a century ago

55 Per patient, all DSA (IgM, IgG3, and IgG) refers to the same serologic specificity.

56 ereas type I IFN responses are controlled by IgG3, and IgG1 is able to regulate both.

57 e to NP-alphaGalCer is dominated by the IgM, IgG3, and IgG2c isotypes, and marginal zone B cells stim

58 able levels of rMal d 1-specific IgG1, IgG2, IgG3, and IgG4 antibodies.

59 ly-useful properties compared with the IgG1, IgG3, and IgG4 antibody subclasses.

60 distinct properties compared with the IgG2, IgG3, and IgG4 subclasses and is the most exploited subc

61 chnology, 5C12 isotype variants (IgG1, IgG2, IgG3, and IgG4) and antibody fragments [Fab, F(ab')(2)]

62 g IgG1 develop earlier and stronger IgG2a/c, IgG3, and IgM responses to L. mexicana infection and yet

63 IgG1, IgG3, and IgM were significantly correlated with C1q fix

64 orrelated with the titer of elicited IgM and IgG3 anti-Cps14.

65 iated with elevated serum levels of IgG2 and IgG3 anti-dsDNA antibodies and accumulation of many IgG

66 epitope density in the wild-type strain, the IgG3 anti-fHbp MAbs had the greatest bactericidal activi

67 prolonged the lives of infected BALB/c mice, IgG3 anti-GXM did not affect animal survival, while mice

68 Monoclonal 6-19 IgG3 anti-IgG2a rheumatoid factor derived from lupus-pro

69 the Ab response after i.v. administration of IgG3 anti-trinitrophenyl (TNP) in complex with OVA-TNP.

70 disease develops when mice are injected with IgG3 anti-trinitrophenyl (TNP) monoclonal antibody follo

71 was confirmed when two of three recombinant IgG3 anti-V2 MAbs were compared to their IgG1 counterpar

72 Furthermore, IgG2a and IgG3 antibodies in the mice were highly somatically muta

73 y IgG4 antibodies, and one patient presented IgG3 antibodies that activated the complement pathway in

74 Anti-V1V2 IgG3 antibodies that were associated with decreased HIV-

75 rospectively test for anti-HLA IgG, IgM, and IgG3 antibodies via LABScreen single-antigen bead assay

76 We report on 2 human IgG3 antibodies with a hinge deletion and a C131S point

77 activity, to the nephritogenic potential of IgG3 antibodies.

78 to the protective immunity observed with the IgG3 antibodies.

79 unoglobulin G1 (IgG1) and immunoglobulin G3 (IgG3) antibodies to antigens diagnostic of recent infect

80 response is dominated by immunoglobulin G3 (IgG3) antibodies.

81 Anti-GD2 murine IgG3 antibody 3F8 kills neuroblastoma cells by antibody-

82 gand Rae-1beta to the 3' end of an anti-HER2 IgG3 antibody containing an intact Fc domain (anti-HER2

83 Toll-like receptor (TLR)-dependent IgG2b and IgG3 antibody responses against their gut microbiota.

84 The response involved predominantly IgG2 and IgG3 antibody subclasses.

85 sponses to capsid also had higher anti-AAV-1 IgG3 antibody titer.

86 t a role for vaccine-elicited anti-HIV-1 Env IgG3, antibody engagement of FcRs, and phagocytosis as p

87 ecific carbohydrate immunoglobulins, namely, IgG3, are generated from intraperitoneal immunizations w

88 onomeric human IgG and its subtypes IgG1 and IgG3 as well as rabbit IgG with on-rates of 6.5 x 10(3),

89 ary boosting, and consisted of only IgG1 and IgG3, as opposed to all four IgG isotypes in response to

90 o a decrease of serum IgG1 and IgG2c but not IgG3, as well as decreased IgM, associated with increase

91 e class switching to IgG1, IgG2a, IgG2b, and IgG3, as well as the formation of germinal centers.

92 d in patients with low viremia who developed IgG3 at a later stage.

93 15.6% were IgG3- at both visits, suggesting absence of recent chlam

94 In this study, we show that both IgG2a and IgG3 autoantibodies are pathogenic in IFN-alpha-accelera

95 rt-lived plasma cells that produce IgG2a and IgG3 autoantibodies.

96 high-dose CTLA4-Ig attenuates both IgG2a and IgG3 autoantibody production and significantly delays de

97 both IgM and class-switched IgG1, IgG2b, and IgG3 autoreactive Abs that depended on the epitope densi

98 Furthermore, cells treated with anti-hTfR IgG3-Av exhibit mitochondrial depolarization and activat

99 l microscopy of cells treated with anti-hTfR IgG3-Av shows that the TfR is directed to an intracellul

100 ceptor IgG3-avidin fusion protein (anti-hTfR IgG3-Av) inhibits the proliferation of an erythroleukemi

101 th induced by anti-TfR Abs such as anti-hTfR IgG3-Av, a molecule that may be useful in the treatment

102 rted that an anti-human transferrin receptor IgG3-avidin fusion protein (anti-hTfR IgG3-Av) inhibits

103 Secondary and exploratory analyses compared IgG3 bAb responses, IgG bAb breadth scores, neutralizing

104 d HIV-1 risk when ADCP, Env-FcgammaRIIa, and IgG3 binding were high.

105 Antibody (IgG, IgG3 binding, and neutralizing) and CD4+ T-cell (express

106 Infant IgG3-binding antibodies were not associated with infecte

107 JAR 3 (IgG3) blocks fH binding and elicits SBA against 2 strain

108 Follow-up analyses revealed that anti-Env IgG3 breadth correlated with reduced HIV-1 risk, anti-En

109 toantigen selection and isotype switching to IgG3 but have minimal effect on end-organ damage or surv

110 tenuated the nephritogenic potential of 6-19 IgG3 by limiting its cryoglobulin activity.

111 IgG3, C1q fixation, and opsonic-phagocytosis seropositiv

112 1q binding site or via generation of an IgG1/IgG3 chimera.

113 ovo DQ-only recipients with AR had more IgG1/IgG3 combination and C1q-binding antibodies (51%, P=0.01

114 ncreased transplacental transfer of GLURP-R2 IgG3 compared to those without the IgG3-H435 allele.

115 ng subclasses IgG1, IgG2a, IgG2b, IgG2c, and IgG3, compared with wild-type mice, which correlated wit

116 The prevalence of IgG3, complement-fixing antibodies, and merozoite phagoc

117 IgG1 and IgG3 comprised the predominant anti-Chlamydia serum anti

118 Of these women, 71.4% were IgG1+IgG3+, consistent with more recent chlamydia resolution.

119 ngth IgG1 and IgG3 mAbs having human IgG1 or IgG3 constant regions.

120 ice and found that the presence of IgG2c and IgG3 correlated with reduced bacterial titers after intr

121 e reproduced in cells treated with anti-hTfR IgG3 cross-linked with a secondary Ab, suggesting that t

122 on and stimulate IgG1 switching but suppress IgG3 CSR.

123 strong induction of IgG1, IgG2a, IgG2b, and IgG3, decrease of specific and total IgE, as well as of

124 q binding affinity compared with human IgG1, IgG3 does not consistently promote superior CML.

125 lar memory response in combination with IgG1/IgG3-dominated humoral immunity that increase with age.

126 underlying molecular mechanisms of IgG1- and IgG3-driven complement activation using isotype variants

127 blood, and their magnitude was predictive of IgG3 DSA generation, more severe allograft injury, and h

128 g immunoglobulin-M (IgM) and IgG subclass 3 (IgG3) DSA to determine if these identify the IgG DSA pat

129 In light of the recognized potency of IgG3 effector mechanisms, we adopted a functional approa

130 ed; conversely, OMP-1-specific huMAb EHRL-4 (IgG3) engaged intracellular TRIM21 and initiated an imme

131 d that recipients treated with anti-CD28-PV1-IgG3 exhibited suppression of alloantigen-initiated prox

132 We conclude that a specific receptor for IgG3 exists in mice that is structurally different from

133 IgG3, followed by IgG1, was the predominant IgG subclass

134 The maternal IgG3 gene was sequenced to identify the IgG3-H435 polymo

135 Murine IgG3 glycan-targeting mAb often induces direct cell kill

136 gG3DeltaHinge:R435H=wild-type IgG1=wild-type IgG3>>>IgG3DeltaHinge, respectively.

137 n an area highly endemic for malaria had the IgG3-H435 allele (377 women homozygous for the IgG3-R435

138 Women with the IgG3-H435 allele had a 78% (95% CI 17%, 170%, p = 0.007)

139 The IgG3-H435 allele may be under positive selection, given

140 -R/H alleles, and 3 women homozygous for the IgG3-H435 allele).

141 GLURP-R2 IgG3 compared to those without the IgG3-H435 allele.

142 Infants born to women with IgG3-H435 had a 32% lower risk of symptomatic malaria du

143 to examine the association between maternal IgG3-H435 polymorphism and transplacental transfer of Ig

144 rnal IgG3 gene was sequenced to identify the IgG3-H435 polymorphism.

145 bility to determine (i) the actual amount of IgG3-H435 relative to IgG-R435 in serum samples and (ii)

146 This study examines the hypotheses that the IgG3-H435 variant promotes increased transplacental tran

147 hermore, in infants born to mothers with the IgG3-H435 variant, a 28% longer IgG3 half-life was noted

148 ria in infants born to women with or without IgG3-H435.

149 malaria-specific antibodies and a prolonged IgG3 half-life in infants and that its presence correlat

150 ers with the IgG3-H435 variant, a 28% longer IgG3 half-life was noted (95% CI 4%, 59%, p = 0.02) comp

151 Some haplotypes of IgG3 have histidine at position 435.

152 subclasses in a Cox survival model revealed IgG3 iDSA and C1q-binding iDSA were strongly and indepen

153 IgG3 iDSA was associated with a shorter time to rejectio

154 bclasses revealed aABMR was mainly driven by IgG3 iDSA, whereas sABMR was driven by IgG4 iDSA.

155 three daily 1-microg doses of anti-HER2/neu-IgG3-IFN-alpha beginning 1 day after tumor challenge res

156 Remarkably, anti-HER2/neu-IgG3-IFN-alpha demonstrated potent activity against esta

157 Anti-HER2/neu-IgG3-IFN-alpha exhibited potent inhibition of 38C13/HER2

158 i-HER2/neu-IgG3 and IFN-alpha (anti-HER2/neu-IgG3-IFN-alpha) and investigated its effect on a murine

159 HIV-1 risk; however, HIV-1 envelope-specific IgG3, IgA; and host FcgammaRIIa genotype also influenced

160 ormal IgG1 and IgE but substantially reduced IgG3, IgG2b, and IgA serum levels.

161 IgM and IgG3 Igs were drastically reduced in the serum of Ikappa

162 y specific for human HER2/neu [anti-HER2/neu IgG3-(IL-2)] was covalently attached to the PMLA backbon

163 sized the important role of malaria-specific IgG3 in malaria immunity, and its transfer may reduce th

164 ding CSR, including a profound deficiency of IgG3 in most mice and long microhomologies at Ig switch

165 Except for IgG3 in the IPPs and mesenteric lymph nodes, no stochast

166 splacental transfer and reduced half-life of IgG3 in vivo.

167 l transfer and half-life of malaria-specific IgG3 in young infants and is associated with reduced ris

168 a blocking anti-CD28 antibody (Anti-CD28-PV1-IgG3) in vitro and in vivo.

169 Ag administered together with specific IgG3 induces a higher Ab response than Ag administered a

170 on of whether a specific receptor exists for IgG3 is critically important for understanding Ab-mediat

171 In contrast to other IgG subclasses, IgG3 is highly polymorphic and usually contains an argin

172 Thus, IgG1, but not IgG2a/c or IgG3, is pathogenic in vivo, in agreement with prior stu

173 ossessed an unusually high proportion of the IgG3 isotype in contrast to Abs induced against foreign

174 C5F2, an IgG3 isotype, recognizes an epitope in the N terminus of

175 PF4/heparin-specific antibodies of IgG2b and IgG3 isotypes.

176 capable of producing antibodies of IgG2b and IgG3 isotypes.

177 es produced by wild-type mice were IgG2b and IgG3 isotypes.

178 The median IgG3 level was highest at 6 months of age.

179 low-dose DMPA decreased glomerular IgG2a and IgG3 levels compared with vehicle treatment.

180 IgG3 levels correlated significantly with IFN-gamma, but

181 y, deletion of Blimp-1 changes neither serum IgG3 levels nor the amount of IgG3 secreted per cell.

182 Survivors had significantly higher anti-Hcp1 IgG3 levels than non-survivors.

183 Moreover, Ag-specific serum IgG3 levels, as well as IgG2c, IgG2b, and IgA levels, re

184 al IgG and IgG1-3 and anti-HLA-total IgG and IgG3 levels, suggesting that TCZ suppresses Ig productio

185 ragine-linked oligosaccharide chains of 6-19 IgG3 mAb are poorly galactosylated and hardly sialylated

186 nsequently, the direct cell killing of mouse IgG3 mAb is lost upon chimerization or humanization.

187 Two IgG3 MAbs against the V2 and V3 regions displayed domina

188 ere both converted into full-length IgG1 and IgG3 mAbs having human IgG1 or IgG3 constant regions.

189 sly reported that anti-Gal-alpha1,3Gal (Gal) IgG3 mAbs mediate a classical complement-dependent hyper

190 ar or greater bactericidal activity than the IgG3 MAbs, and the activity was less dependent on the in

191 ainst a wild-type group B isolate, all three IgG3 MAbs, irrespective of their ability to inhibit fH b

192 ilar or greater activity than the respective IgG3 MAbs.

193 Absence of early CHIKV-specific IgG3 may therefore serve as a specific marker of patient

194 e necessity and sufficiency of complement in IgG3-mediated HAR and the necessity of both complement a

195 Like IgG1, IgG3-mediated phagocytosis was associated with fungal re

196 visited this question by analyzing IgG1- and IgG3-mediated phagocytosis with variable region-identica

197 32A(R) not only to IgG2 but also to IgG1 and IgG3 might be responsible for the lack of clearance of I

198 s first identified with an anti-carbohydrate IgG3 monoclonal antibody called WIC29.26 and has been sh

199 ups, but IgM was predominant in children and IgG3 more prevalent in adults.

200 cell subsets, we detected elevated levels of IgG3 natural Abs and a striking increase of T-independen

201 CML triggered by anti-EGFR-IgG3 negatively correlated with expression levels of the

202 s, while other Ig classes were not (IgG1 and IgG3) or much less so (IgG2b, IgA).

203 (P = .025), AMA1 IgG1 (P = .001), and EBA175 IgG3 (P = .001).

204 (P = .002), lysate IgG1 (P = .001), and MSP1 IgG3 (P = .01).

205 with reduced CMR of MSP1 IgG1 (P = .022) and IgG3 (P = .023), lysate IgG1 (P = .027) and IgG3 (P = .0

206 IgG3 (P = .023), lysate IgG1 (P = .027) and IgG3 (P = .025), AMA1 IgG1 (P = .001), and EBA175 IgG3 (

207 n controls (immunoglobulin [Ig]G1, P < .001; IgG3, P < .001).

208 Patients with IgM persistent IgG3 positive DSA (n=19) were more likely to have allogr

209 We found that development of IgM persistent IgG3 positive DSA identifies the most dangerous IgG DSA

210 sted in 33 patients and an isotype switch to IgG3 positive DSA occurred in 25 patients.

211 ed with DSA mean fluorescence intensity, DSA IgG3 positivity and C1q binding capacity adequately recl

212 Addition of DSA IgG3 positivity or C1q binding capacity increased discri

213 correlated with the loss of either IgG1 and IgG3, possibly because of certain manufacturing procedur

214 ) showed reduction of anti-HLA-total IgG and IgG3 post-TCZ, but this was not statistically significan

215 yte-selective injury model NEP25 mice and an IgG3-producing hybridoma clone 2B11.3 established by MRL

216 -B6.1 that produces protective antibody, the IgG3-producing hybridoma, and a nonprotective IgG1-produ

217 d for the enhanced production of Ag-specific IgG3 production in the CD21/35(-/-) mouse compared with

218 A reduction in IgG3 production was also noted with a thymus-independent

219 n-specific immunoglobulin M (IgM), IgG1, and IgG3 production.

220 Notably, anti-EGFR-IgG3 promoted strong C1q and C3b, but relatively low C4b

221 ed to investigate the glycosylation of human IgG3 providing details on the hitherto uncharacterized g

222 -R435 allele, 117 women heterozygous for the IgG3-R/H alleles, and 3 women homozygous for the IgG3-H4

223 G3-H435 allele (377 women homozygous for the IgG3-R435 allele, 117 women heterozygous for the IgG3-R/

224 o infants born to mothers homozygous for the IgG3-R435 allele.

225 ed to infants born to mothers homozygous for IgG3-R435.

226 dy containing an intact Fc domain (anti-HER2 IgG3-Rae-1beta), thereby targeting an NK cell activation

227 ion changed over time, with IgG1 persisting, IgG3 rapidly declining, and IgG4 appearing late.

228 ) -targeting 88mAb, we identified the murine IgG3 residues underlying the direct cell killing and inc

229 hrocyte lysis was observed with the IgG1 and IgG3, respectively, but no increase with IgG2 and IgG4 a

230 esponse switched from an IgG1 response to an IgG3 response after infection with L. interrogans Histol

231 esponses, PD-1 induction, and PPS-3-specific IgG3 responses and restored protection during S. pneumon

232 IgG, IgG1, and IgG3 responses generally increased with age, were higher

233 kade also selectively rescued PPS-3-specific IgG3 responses in CD21/35(-/-) mice.

234 articles also elicited IgM, IgG1, IgG2b, and IgG3 responses that were comparable in magnitudes to wil

235 yte-derived DCs enhanced NP-specific IgM and IgG3 responses to NP-Ficoll.

236 The magnitude of the IgG1 and IgG3 responses was greatest in female and African Americ

237 While IgG3 responses were highest in T3, a lower IgA/IgG ratio

238 IgE responses and did not affect IgG2a/c and IgG3 responses.

239 ng an assay that measured immunoglobulin G3 (IgG3) responses against ZIKV NS1 antigen, we estimated t

240 Allotypic variation in IgG3 resulted in widely different CH3 interaction streng

241 ed and two distinct more galactosylated 6-19 IgG3 rheumatoid factor variants.

242 yogenic and nephritogenic activities of 6-19 IgG3 rheumatoid factor, terminal sialylation attenuated

243 ributing to the pathogenic potential of 6-19 IgG3 rheumatoid factors.

244 neither serum IgG3 levels nor the amount of IgG3 secreted per cell.

245 of both splenic and bone marrow Ag-specific IgG3-secreting cells, but not IgM-secreting cells, at bo

246 ective production of IgG1 and IgG2b, but not IgG3 serum Ab, accompanied by reductions in long-lived b

247 long-lived response) and immunoglobulin G3 (IgG3; short-lived response indicating more recent infect

248 hese results imply that human IgG1 and human IgG3 should have a greater capacity to trigger monocyte

249 onfocal analysis of anti-PLA2R and antihuman IgG3 showed co-localization, and the patient had IgG3kap

250 Titers of IgG4, but not IgG1 or IgG3, significantly correlated with the occurrence of sp

251 samples were assayed for levels of IgG1 and IgG3 specific for MSP119, MSP2 (both allelic families, 3

252 = 0.02) especially if the HLA DSA was of the IgG3 subclass (HR, 2.28; P = 0.01).

253 Antigen-specific IgG3 subclass antibodies were quantified in the same sam

254 region of gp120, in particular the IgG1 and IgG3 subclass mediating antibody-dependent cell-mediated

255 The IgG3 subclass response was higher in AF fractions from D

256 h mean fluorescence intensity, rarely of the IgG3 subclass, and often capable of binding C1q.

257 ermline precursors, are often from the minor IgG3 subclass, and some are polyreactive, such as 4E10.

258 FI]>500), strong complement-binding IgG1 and IgG3 subclasses accounted for a median of 99% (interquar

259 g likely because complement-binding IgG1 and IgG3 subclasses dominate regarding frequency and relativ

260 IgG1 and IgG3 subclasses of IgG are potent effectors of complemen

261 s, and in vivo efficacies, with the IgG1 and IgG3 subclasses reacting similarly.

262 ntibody production predominantly of IgG1 and IgG3 subclasses.

263 properties compared with the IgG1, IgG2, and IgG3 subclasses.

264 dies with strong complement-binding IgG1 and IgG3 subclasses.

265 sera is predominantly restricted to IgG1 and IgG3 subclasses.

266 rential isotype class switching to IgG2a and IgG3 subtypes.

267 not only to human IgG2, but also to IgG1 and IgG3 subtypes.

268 eraction strengths that were even weaker for IgG3 than for IgG4 in the case of allotype G3m(c3c5*/6,2

269 revalence of cytophilic antibodies (IgG1 and IgG3), that seem to have an essential role in protective

270 G1 during its normal life span; for IgG2 and IgG3 the inter-heavy chain disulfide bonds are essential

271 ependent cellular phagocytosis, Env-specific IgG3, tier 1A neutralising activity, and broad cellular

272 lations occurred, resulting in increased IgM/IgG3 titers to the oxidation-specific epitopes.

273 essed in the presence of CD55, forcing human IgG3 to act mainly through the alternative pathway.

274 ment at residue 435 in the binding domain of IgG3 to FcRn increases the transplacental transfer and h

275 t in the IgG subclass profile from IgG2a and IgG3 to IgG1 in the sd-tg MRL-lpr mice.

276 d by combining an engineered hinge domain of IgG3 to increase Fab domain flexibility necessary for he

277 The age and tissue dependence of IgG3 transcription paralleled the developmental persiste

278 Furthermore, anti-EGFR-IgG3 triggered C4a release on all cells but failed to in

279 CML of investigated target cells, anti-EGFR-IgG3 triggered significant CML of some, but not all test

280 ion to be a pivotal determinant of anti-EGFR-IgG3-triggered CML and to force a switch from classical

281 lence range, 5%-35% for IgG1 and 27%-41% for IgG3), varied across study sites, and was lowest in stud

282 We describe full-length IgG2b and IgG3 versions of JM4 that target the coreceptor-binding

283 with ~1 muM KD, whereas the interaction with IgG3 was a magnitude weaker.

284 IgG3 was an efficient opsonin for C. neoformans in Fcgam

285 y, while production of cat-specific IgG1 and IgG3 was not stimulated by MAT-Feld1 ILIT.

286 Almost 3 decades ago, murine IgG3 was proposed to interact with a different receptor

287 the antimerozoite-specific antibodies, only IgG3 was significantly associated with both OP and prote

288 Switching to IgG3 was significantly reduced in IkappaBNS KO B cells.

289 Anti-DNA IgG3 was the unique non-IgG2 anti-DNA deposit, and anti-

290 IgG1, IgG2a, and IgG2b, but not by anti-Gal IgG3, was dependent on FcgammaRI.

291 The effects of IgG3 were dependent on CR1/2 known to be expressed on B

292 IgG1, IgG2a, and IgG3 were raised against epitope-bearing fibrils in leve

293 on and gene usage in VH regions of IgG2a and IgG3 were studied by single-cell polymerase chain reacti

294 isotype switching to IgG1, IgG2b, IgG2c, and IgG3 were the same as C57BL/6 control cells.

295 ted mice had less antipneumococcal IgG2c and IgG3, were less efficient at inducing opsonophagocytic k

296 Humoral immunity was dominated by IgG1 and IgG3, whereas the Th2-associated IgG4 isotype was only d

297 imals is depressed production of Ag-specific IgG3 which we show is evident in vivo but not in vitro.

298 IgG3, which self-associates to form large immune complex

299 resulted in impaired ex vivo CSR to IgG1 and IgG3, which was associated with reduced mutation frequen

300 on of the binding of IgG1, IgG2a, IgG2b, and IgG3 with a 12-mer peptide mimetic of Cryptococcus neofo