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1 s were each paired with human IgG1, IgG2, or IgG3.
2 ount for near-normal levels of serum IgM and IgG3.
3 th up to 50-fold increases in serum IgG1 and IgG3.
4 showed higher levels of anti-MDA-LDL IgM and IgG3.
5 reases in all subtypes with the exception of IgG3.
6 ns of all Ig isotypes were low, particularly IgG3.
7 ndent on FcgammaRIII, with IgG1>IgG2b>>IgG2a=IgG3.
8 -1 and MSP-1(42) were predominantly IgG1 and IgG3.
9 hways with a hierarchy of IgG2a/c>IgG1/IgG2b>IgG3.
10 By contrast, human CD16 binds to IgG1 and IgG3.
11 pr mice of any H2 type with detectable serum IgG3.
12 lative protective efficacy of IgG1, IgG2a >> IgG3.
13 -1(neg) B-1 cells are also a major source of IgG3.
14 red by the presence of LTP-specific IgG1 and IgG3.
15 ered the production of IFN-gamma, IgG2a, and IgG3.
16 plasma cells and reduced levels of IgG2b and IgG3.
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
29 polymorphism and transplacental transfer of IgG3, adjusting for hypergammaglobulinemia, maternal mal
30 , we demonstrate that an optimal response to IgG3-Ag complexes requires that CR1/2 is expressed on bo
31 a suggest that CR1/2(+) MZ B cells transport IgG3-Ag-C complexes from the MZ to the follicles, where
32 studies of IgG subclass responses identified IgG3 against a peptide derived from MSP3 as the stronges
35 other with low-to-moderate-affinity IgG1 and IgG3 also later developed low-titer FVIII inhibitors.
36 Together, these data suggest human anti-EGFR-IgG3, although highly reactive with C1q, to weakly promo
37 protection against malaria and further shows IgG3 and GLURP antibodies are key in the OP mechanism, t
38 switch slightly better to IgG2a, IgG2b, and IgG3 and have more S region DSBs and mutations than wild
39 a fusion protein consisting of anti-HER2/neu-IgG3 and IFN-alpha (anti-HER2/neu-IgG3-IFN-alpha) and in
42 nover rate during activation of switching to IgG3 and IgG2b, as well as delays in CSR kinetics associ
43 ariants showed protection in vitro, with the IgG3 and IgG4 variants showing the highest protection in
44 quence with those of other subclasses (IgG2, IgG3 and IgG4) showed that these aggregation-prone motif
45 estingly, the F240 isotype-switched variants IgG3 and IgG4, also expressed in CHO cells, exhibited id
49 40, mostly low-to-moderate-affinity IgG1 and IgG3, and 1 had high-affinity IgG4 and later developed l
50 uced glomerular accumulation of IgG1, IgG2a, IgG3, and complement, while low-dose DMPA decreased glom
51 splacental transport with wild-type IgG1 and IgG3, and found transport across trophoblast-derived BeW
52 uced titers of secreted class-switched IgG1, IgG3, and IgA antibodies, without alterations in critica
53 autoantibodies were skewed toward the IgG1, IgG3, and IgA isotypes, probably recognizing a tertiary
56 ecreted substantially less IgA, IgG1, IgG2a, IgG3, and IgE than wild-type (WT) controls in response t
59 e to NP-alphaGalCer is dominated by the IgM, IgG3, and IgG2c isotypes, and marginal zone B cells stim
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)]
63 g IgG1 develop earlier and stronger IgG2a/c, IgG3, and IgM responses to L. mexicana infection and yet
65 in G2a (IgG2a) and IgG2b, but not of IgG1 or IgG3, and the ability of sera from immunized animals to
67 iated with elevated serum levels of IgG2 and IgG3 anti-dsDNA antibodies and accumulation of many IgG
68 epitope density in the wild-type strain, the IgG3 anti-fHbp MAbs had the greatest bactericidal activi
69 prolonged the lives of infected BALB/c mice, IgG3 anti-GXM did not affect animal survival, while mice
71 the Ab response after i.v. administration of IgG3 anti-trinitrophenyl (TNP) in complex with OVA-TNP.
72 disease develops when mice are injected with IgG3 anti-trinitrophenyl (TNP) monoclonal antibody follo
73 was confirmed when two of three recombinant IgG3 anti-V2 MAbs were compared to their IgG1 counterpar
75 y IgG4 antibodies, and one patient presented IgG3 antibodies that activated the complement pathway in
78 rospectively test for anti-HLA IgG, IgM, and IgG3 antibodies via LABScreen single-antigen bead assay
81 unoglobulin G1 (IgG1) and immunoglobulin G3 (IgG3) antibodies to antigens diagnostic of recent infect
84 gand Rae-1beta to the 3' end of an anti-HER2 IgG3 antibody containing an intact Fc domain (anti-HER2
85 Toll-like receptor (TLR)-dependent IgG2b and IgG3 antibody responses against their gut microbiota.
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
94 In this study, we show that both IgG2a and IgG3 autoantibodies are pathogenic in IFN-alpha-accelera
96 high-dose CTLA4-Ig attenuates both IgG2a and IgG3 autoantibody production and significantly delays de
98 Furthermore, cells treated with anti-hTfR IgG3-Av exhibit mitochondrial depolarization and activat
101 l microscopy of cells treated with anti-hTfR IgG3-Av shows that the TfR is directed to an intracellul
102 ceptor IgG3-avidin fusion protein (anti-hTfR IgG3-Av) inhibits the proliferation of an erythroleukemi
103 th induced by anti-TfR Abs such as anti-hTfR IgG3-Av, a molecule that may be useful in the treatment
104 rted that an anti-human transferrin receptor IgG3-avidin fusion protein (anti-hTfR IgG3-Av) inhibits
107 toantigen selection and isotype switching to IgG3 but have minimal effect on end-organ damage or surv
110 ovo DQ-only recipients with AR had more IgG1/IgG3 combination and C1q-binding antibodies (51%, P=0.01
112 ncreased transplacental transfer of GLURP-R2 IgG3 compared to those without the IgG3-H435 allele.
113 ng subclasses IgG1, IgG2a, IgG2b, IgG2c, and IgG3, compared with wild-type mice, which correlated wit
117 ice and found that the presence of IgG2c and IgG3 correlated with reduced bacterial titers after intr
118 e reproduced in cells treated with anti-hTfR IgG3 cross-linked with a secondary Ab, suggesting that t
119 precipitate in C57BL/6 mice consisted of the IgG3 cryoglobulin only (type I cryoglobulinemia) compare
120 jection of 6-19 hybridoma cells producing an IgG3 cryoglobulin with rheumatoid factor activity agains
122 of MRL/lpr H2b/b mice were found to be serum IgG3 deficient (with few to no IgG3-producing B cells).
126 lar memory response in combination with IgG1/IgG3-dominated humoral immunity that increase with age.
127 relationship between IgG1, IgG2a, IgG2b, and IgG3 dose, infective inocula, and protection was investi
128 underlying molecular mechanisms of IgG1- and IgG3-driven complement activation using isotype variants
129 g immunoglobulin-M (IgM) and IgG subclass 3 (IgG3) DSA to determine if these identify the IgG DSA pat
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
135 n an area highly endemic for malaria had the IgG3-H435 allele (377 women homozygous for the IgG3-R435
141 to examine the association between maternal IgG3-H435 polymorphism and transplacental transfer of Ig
143 bility to determine (i) the actual amount of IgG3-H435 relative to IgG-R435 in serum samples and (ii)
144 This study examines the hypotheses that the IgG3-H435 variant promotes increased transplacental tran
145 hermore, in infants born to mothers with the IgG3-H435 variant, a 28% longer IgG3 half-life was noted
148 malaria-specific antibodies and a prolonged IgG3 half-life in infants and that its presence correlat
149 ers with the IgG3-H435 variant, a 28% longer IgG3 half-life was noted (95% CI 4%, 59%, p = 0.02) comp
150 wever in the presence of specific Ag, murine IgG3 has been shown to polymerize through noncovalent in
152 Insertion of a cysteine-rich 15-amino acid IgG3 hinge motif (CPEPKSCDTPPPCPR) in both of these muta
153 subclasses in a Cox survival model revealed IgG3 iDSA and C1q-binding iDSA were strongly and indepen
156 three daily 1-microg doses of anti-HER2/neu-IgG3-IFN-alpha beginning 1 day after tumor challenge res
159 i-HER2/neu-IgG3 and IFN-alpha (anti-HER2/neu-IgG3-IFN-alpha) and investigated its effect on a murine
160 only (type I cryoglobulinemia) compared with IgG3-IgG2a complexes in BALB/c (type II cryoglobulinemia
161 n involved most IgG1, but also a fraction of IgG3-, IgG2a-, IgG2b-, and IgA-expressing GC and post-GC
163 fects in elicitation of type 1 IgG isotypes (IgG3, IgG2b, and IgG2a), but not the type 2 IgG isotype,
164 (SWA)-specific immunoglobulin (Ig) G1, IgG2, IgG3, IgG4, interleukin (IL)-4, and IL-5 increased signi
166 y specific for human HER2/neu [anti-HER2/neu IgG3-(IL-2)] was covalently attached to the PMLA backbon
167 sized the important role of malaria-specific IgG3 in malaria immunity, and its transfer may reduce th
168 ding CSR, including a profound deficiency of IgG3 in most mice and long microhomologies at Ig switch
170 amount of antigen-specific IgG1, IgG2b, and IgG3 in the serum and more IgG2b and IgG3 deposited with
172 l transfer and half-life of malaria-specific IgG3 in young infants and is associated with reduced ris
175 on of whether a specific receptor exists for IgG3 is critically important for understanding Ab-mediat
177 e now report that in C57BL/6J x 129/Sv mice, IgG3 is protective while IgG1 is not protective, with ne
181 ossessed an unusually high proportion of the IgG3 isotype in contrast to Abs induced against foreign
182 L(266-280)/PDC-E2(212-226) reactivity of the IgG3 isotype was found in 52 (52%) AMA-positive PBC pati
190 y, deletion of Blimp-1 changes neither serum IgG3 levels nor the amount of IgG3 secreted per cell.
192 ragine-linked oligosaccharide chains of 6-19 IgG3 mAb are poorly galactosylated and hardly sialylated
195 ere both converted into full-length IgG1 and IgG3 mAbs having human IgG1 or IgG3 constant regions.
196 sly reported that anti-Gal-alpha1,3Gal (Gal) IgG3 mAbs mediate a classical complement-dependent hyper
197 ar or greater bactericidal activity than the IgG3 MAbs, and the activity was less dependent on the in
198 ainst a wild-type group B isolate, all three IgG3 MAbs, irrespective of their ability to inhibit fH b
200 We hypothesize that long-hinged porcine IgG3 may be important in preadaptive responses to T cell
202 e necessity and sufficiency of complement in IgG3-mediated HAR and the necessity of both complement a
204 visited this question by analyzing IgG1- and IgG3-mediated phagocytosis with variable region-identica
205 the genetic background of the host and that IgG3-mediated protection in C57BL/6J x 129/Sv mice was a
206 32A(R) not only to IgG2 but also to IgG1 and IgG3 might be responsible for the lack of clearance of I
207 s first identified with an anti-carbohydrate IgG3 monoclonal antibody called WIC29.26 and has been sh
208 cell subsets, we detected elevated levels of IgG3 natural Abs and a striking increase of T-independen
210 pe of anti-HER2 antibodies was predominantly IgG3 of low avidity, suggesting a Th1 response to peptid
211 Administration of either a chimeric (NM-IgG3) or digestion product (NM-F(ab')2) form of the anti
215 with reduced CMR of MSP1 IgG1 (P = .022) and IgG3 (P = .023), lysate IgG1 (P = .027) and IgG3 (P = .0
216 IgG3 (P = .023), lysate IgG1 (P = .027) and IgG3 (P = .025), AMA1 IgG1 (P = .001), and EBA175 IgG3 (
218 We found that development of IgM persistent IgG3 positive DSA identifies the most dangerous IgG DSA
220 ed with DSA mean fluorescence intensity, DSA IgG3 positivity and C1q binding capacity adequately recl
222 correlated with the loss of either IgG1 and IgG3, possibly because of certain manufacturing procedur
224 -B6.1 that produces protective antibody, the IgG3-producing hybridoma, and a nonprotective IgG1-produ
225 d for the enhanced production of Ag-specific IgG3 production in the CD21/35(-/-) mouse compared with
229 ed to investigate the glycosylation of human IgG3 providing details on the hitherto uncharacterized g
230 -R435 allele, 117 women heterozygous for the IgG3-R/H alleles, and 3 women homozygous for the IgG3-H4
231 G3-H435 allele (377 women homozygous for the IgG3-R435 allele, 117 women heterozygous for the IgG3-R/
234 dy containing an intact Fc domain (anti-HER2 IgG3-Rae-1beta), thereby targeting an NK cell activation
235 hrocyte lysis was observed with the IgG1 and IgG3, respectively, but no increase with IgG2 and IgG4 a
236 esponse switched from an IgG1 response to an IgG3 response after infection with L. interrogans Histol
237 esponses, PD-1 induction, and PPS-3-specific IgG3 responses and restored protection during S. pneumon
245 yogenic and nephritogenic activities of 6-19 IgG3 rheumatoid factor, terminal sialylation attenuated
248 of both splenic and bone marrow Ag-specific IgG3-secreting cells, but not IgM-secreting cells, at bo
250 ective production of IgG1 and IgG2b, but not IgG3 serum Ab, accompanied by reductions in long-lived b
251 long-lived response) and immunoglobulin G3 (IgG3; short-lived response indicating more recent infect
252 hese results imply that human IgG1 and human IgG3 should have a greater capacity to trigger monocyte
253 onfocal analysis of anti-PLA2R and antihuman IgG3 showed co-localization, and the patient had IgG3kap
255 samples were assayed for levels of IgG1 and IgG3 specific for MSP119, MSP2 (both allelic families, 3
257 region of gp120, in particular the IgG1 and IgG3 subclass mediating antibody-dependent cell-mediated
260 FI]>500), strong complement-binding IgG1 and IgG3 subclasses accounted for a median of 99% (interquar
261 g likely because complement-binding IgG1 and IgG3 subclasses dominate regarding frequency and relativ
268 eraction strengths that were even weaker for IgG3 than for IgG4 in the case of allotype G3m(c3c5*/6,2
269 G1 during its normal life span; for IgG2 and IgG3 the inter-heavy chain disulfide bonds are essential
270 d HPV16 VLP-specific IgG1, IgG2a, IgG2b, and IgG3 titers after vaccination as compared with the contr
272 essed in the presence of CD55, forcing human IgG3 to act mainly through the alternative pathway.
273 ment at residue 435 in the binding domain of IgG3 to FcRn increases the transplacental transfer and h
275 d by combining an engineered hinge domain of IgG3 to increase Fab domain flexibility necessary for he
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
287 the antimerozoite-specific antibodies, only IgG3 was significantly associated with both OP and prote
293 on and gene usage in VH regions of IgG2a and IgG3 were studied by single-cell polymerase chain reacti
295 immunoglobulin G2a [IgG2a] >> IgG1 = IgG2b > IgG3) were significantly higher than pneumococcal surfac
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.
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
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