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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.
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         Most surprising was the finding that IgG3 accounted for half of all Cgamma transcripts in the
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
33  prevalent in LN serum, which also contained IgG3 against the antigen panel and anti-C1q IgG4.
34 6.1 (an immunoglobulin M [IgM]) and C3.1 (an IgG3) against experimental candidiasis.
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
40  but displayed significantly lower levels of IgG3 and IFN-gamma compared with adults.
41 fectively elicits class-switched NP-specific IgG3 and IgG2b in mice.
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
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 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
54      Natural Abs, belonging to isotypes IgM, IgG3, and IgA, were discovered nearly half a century ago
55 s, the most consistently detected were IgG1, IgG3, and IgA.
56 ecreted substantially less IgA, IgG1, IgG2a, IgG3, and IgE than wild-type (WT) controls in response t
57                   Per patient, all DSA (IgM, IgG3, and IgG) refers to the same serologic specificity.
58 s14 responses composed predominantly of IgM, IgG3, and IgG1.
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)]
62 idase activity were obtained for IgG1, IgG2, IgG3, and IgG4.
63 g IgG1 develop earlier and stronger IgG2a/c, IgG3, and IgM responses to L. mexicana infection and yet
64 ially less Ag-specific IgA, IgG1, IgG2b, and IgG3, and less total IgE than Atm+/+ controls.
65 in G2a (IgG2a) and IgG2b, but not of IgG1 or IgG3, and the ability of sera from immunized animals to
66 orrelated with the titer of elicited IgM and IgG3 anti-Cps14.
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
70                              Monoclonal 6-19 IgG3 anti-IgG2a rheumatoid factor derived from lupus-pro
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
74                       Furthermore, IgG2a and IgG3 antibodies in the mice were highly somatically muta
75 y IgG4 antibodies, and one patient presented IgG3 antibodies that activated the complement pathway in
76                                    Anti-V1V2 IgG3 antibodies that were associated with decreased HIV-
77                               In conclusion, IgG3 antibodies to BGAL LACDE cross-react with the major
78 rospectively test for anti-HLA IgG, IgM, and IgG3 antibodies via LABScreen single-antigen bead assay
79                         We report on 2 human IgG3 antibodies with a hinge deletion and a C131S point
80  activity, to the nephritogenic potential of IgG3 antibodies.
81 unoglobulin G1 (IgG1) and immunoglobulin G3 (IgG3) antibodies to antigens diagnostic of recent infect
82  response is dominated by immunoglobulin G3 (IgG3) antibodies.
83                              Anti-GD2 murine IgG3 antibody 3F8 kills neuroblastoma cells by antibody-
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.
86 sponses to capsid also had higher anti-AAV-1 IgG3 antibody titer.
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             We have now found that anti-hTfR IgG3-Av also inhibits the proliferation of additional hu
98    Furthermore, cells treated with anti-hTfR IgG3-Av exhibit mitochondrial depolarization and activat
99                                    Anti-hTfR IgG3-Av induces internalization and rapid degradation of
100         These results suggest that anti-hTfR IgG3-Av induces lethal iron deprivation, but the resulti
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
105                                       Infant IgG3-binding antibodies were not associated with infecte
106                                       JAR 3 (IgG3) blocks fH binding and elicits SBA against 2 strain
107 toantigen selection and isotype switching to IgG3 but have minimal effect on end-organ damage or surv
108 tenuated the nephritogenic potential of 6-19 IgG3 by limiting its cryoglobulin activity.
109 1q binding site or via generation of an IgG1/IgG3 chimera.
110 ovo DQ-only recipients with AR had more IgG1/IgG3 combination and C1q-binding antibodies (51%, P=0.01
111 hibits B cell isotype switching to IgG2a and IgG3, commonly induced by Th1-type cytokines.
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
114                                     IgG1 and IgG3 comprised the predominant anti-Chlamydia serum anti
115              Of these women, 71.4% were IgG1+IgG3+, consistent with more recent chlamydia resolution.
116 ngth IgG1 and IgG3 mAbs having human IgG1 or IgG3 constant regions.
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
121 on and stimulate IgG1 switching but suppress IgG3 CSR.
122 of MRL/lpr H2b/b mice were found to be serum IgG3 deficient (with few to no IgG3-producing B cells).
123                           In addition, H2b/b IgG3-deficient MRL/lpr mice had significantly less prote
124 2b, and IgG3 in the serum and more IgG2b and IgG3 deposited within the glomerulus.
125 q binding affinity compared with human IgG1, IgG3 does not consistently promote superior CML.
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
130        In light of the recognized potency of IgG3 effector mechanisms, we adopted a functional approa
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                                 The maternal IgG3 gene was sequenced to identify the IgG3-H435 polymo
134 gG3DeltaHinge:R435H=wild-type IgG1=wild-type IgG3>>>IgG3DeltaHinge, respectively.
135 n an area highly endemic for malaria had the IgG3-H435 allele (377 women homozygous for the IgG3-R435
136                               Women with the IgG3-H435 allele had a 78% (95% CI 17%, 170%, p = 0.007)
137                                          The IgG3-H435 allele may be under positive selection, given
138 -R/H alleles, and 3 women homozygous for the IgG3-H435 allele).
139  GLURP-R2 IgG3 compared to those without the IgG3-H435 allele.
140                   Infants born to women with IgG3-H435 had a 32% lower risk of symptomatic malaria du
141  to examine the association between maternal IgG3-H435 polymorphism and transplacental transfer of Ig
142 rnal IgG3 gene was sequenced to identify the IgG3-H435 polymorphism.
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
146 ria in infants born to women with or without IgG3-H435.
147                             IgG1, IgG2a, and IgG3 had different effects on IFN-gamma expression in in
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
151                           Some haplotypes of IgG3 have histidine at position 435.
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
154                                              IgG3 iDSA was associated with a shorter time to rejectio
155 bclasses revealed aABMR was mainly driven by IgG3 iDSA, whereas sABMR was driven by IgG4 iDSA.
156  three daily 1-microg doses of anti-HER2/neu-IgG3-IFN-alpha beginning 1 day after tumor challenge res
157                    Remarkably, anti-HER2/neu-IgG3-IFN-alpha demonstrated potent activity against esta
158                                Anti-HER2/neu-IgG3-IFN-alpha exhibited potent inhibition of 38C13/HER2
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
162 ormal IgG1 and IgE but substantially reduced IgG3, IgG2b, and IgA serum levels.
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
165                                      IgM and IgG3 Igs were drastically reduced in the serum of Ikappa
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
169                                   Except for IgG3 in the IPPs and mesenteric lymph nodes, no stochast
170  amount of antigen-specific IgG1, IgG2b, and IgG3 in the serum and more IgG2b and IgG3 deposited with
171 splacental transfer and reduced half-life of IgG3 in vivo.
172 l transfer and half-life of malaria-specific IgG3 in young infants and is associated with reduced ris
173 a blocking anti-CD28 antibody (Anti-CD28-PV1-IgG3) in vitro and in vivo.
174       Ag administered together with specific IgG3 induces a higher Ab response than Ag administered a
175 on of whether a specific receptor exists for IgG3 is critically important for understanding Ab-mediat
176         In contrast to other IgG subclasses, IgG3 is highly polymorphic and usually contains an argin
177 e now report that in C57BL/6J x 129/Sv mice, IgG3 is protective while IgG1 is not protective, with ne
178               Thus, IgG1, but not IgG2a/c or IgG3, is pathogenic in vivo, in agreement with prior stu
179 significant enhancement of parasite-specific IgG3 isotype antibodies.
180 -/- mice also had enhanced parasite-specific IgG3 isotype antibodies.
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
183                                     C5F2, an IgG3 isotype, recognizes an epitope in the N terminus of
184 PF4/heparin-specific antibodies of IgG2b and IgG3 isotypes.
185 capable of producing antibodies of IgG2b and IgG3 isotypes.
186 es produced by wild-type mice were IgG2b and IgG3 isotypes.
187                                   The median IgG3 level was highest at 6 months of age.
188 low-dose DMPA decreased glomerular IgG2a and IgG3 levels compared with vehicle treatment.
189                                              IgG3 levels correlated significantly with IFN-gamma, but
190 y, deletion of Blimp-1 changes neither serum IgG3 levels nor the amount of IgG3 secreted per cell.
191                  Moreover, Ag-specific serum IgG3 levels, as well as IgG2c, IgG2b, and IgA levels, re
192 ragine-linked oligosaccharide chains of 6-19 IgG3 mAb are poorly galactosylated and hardly sialylated
193                     In contrast, an anti-Gal IgG3 mAb induced classic, hyperacute rejection that was
194                                          Two IgG3 MAbs against the V2 and V3 regions displayed domina
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
199 ilar or greater activity than the respective IgG3 MAbs.
200      We hypothesize that long-hinged porcine IgG3 may be important in preadaptive responses to T cell
201              Absence of early CHIKV-specific IgG3 may therefore serve as a specific marker of patient
202 e necessity and sufficiency of complement in IgG3-mediated HAR and the necessity of both complement a
203                                   Like IgG1, IgG3-mediated phagocytosis was associated with fungal re
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
209                   CML triggered by anti-EGFR-IgG3 negatively correlated with expression levels of the
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
212 s, while other Ig classes were not (IgG1 and IgG3) or much less so (IgG2b, IgA).
213 (P = .025), AMA1 IgG1 (P = .001), and EBA175 IgG3 (P = .001).
214 (P = .002), lysate IgG1 (P = .001), and MSP1 IgG3 (P = .01).
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 (
217                 Patients with IgM persistent IgG3 positive DSA (n=19) were more likely to have allogr
218  We found that development of IgM persistent IgG3 positive DSA identifies the most dangerous IgG DSA
219 sted in 33 patients and an isotype switch to IgG3 positive DSA occurred in 25 patients.
220 ed with DSA mean fluorescence intensity, DSA IgG3 positivity and C1q binding capacity adequately recl
221                              Addition of DSA IgG3 positivity or C1q binding capacity increased discri
222  correlated with the loss of either IgG1 and IgG3, possibly because of certain manufacturing procedur
223 d to be serum IgG3 deficient (with few to no IgG3-producing B cells).
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
226                               A reduction in IgG3 production was also noted with a thymus-independent
227 n-specific immunoglobulin M (IgM), IgG1, and IgG3 production.
228                           Notably, anti-EGFR-IgG3 promoted strong C1q and C3b, but relatively low C4b
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/
232 o infants born to mothers homozygous for the IgG3-R435 allele.
233 ed to infants born to mothers homozygous for IgG3-R435.
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
238                               IgG, IgG1, and IgG3 responses generally increased with age, were higher
239 kade also selectively rescued PPS-3-specific IgG3 responses in CD21/35(-/-) mice.
240 yte-derived DCs enhanced NP-specific IgM and IgG3 responses to NP-Ficoll.
241                The magnitude of the IgG1 and IgG3 responses was greatest in female and African Americ
242 IgA responses and T-independent (TI) IgM and IgG3 responses.
243                       Allotypic variation in IgG3 resulted in widely different CH3 interaction streng
244 ed and two distinct more galactosylated 6-19 IgG3 rheumatoid factor variants.
245 yogenic and nephritogenic activities of 6-19 IgG3 rheumatoid factor, terminal sialylation attenuated
246 ributing to the pathogenic potential of 6-19 IgG3 rheumatoid factors.
247  neither serum IgG3 levels nor the amount of IgG3 secreted per cell.
248  of both splenic and bone marrow Ag-specific IgG3-secreting cells, but not IgM-secreting cells, at bo
249 n and promote 50- to 100-fold higher IgM and IgG3 secretion in lupus B cells than in controls.
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
254              Titers of IgG4, but not IgG1 or IgG3, significantly correlated with the occurrence of sp
255  samples were assayed for levels of IgG1 and IgG3 specific for MSP119, MSP2 (both allelic families, 3
256 = 0.02) especially if the HLA DSA was of the IgG3 subclass (HR, 2.28; P = 0.01).
257  region of gp120, in particular the IgG1 and IgG3 subclass mediating antibody-dependent cell-mediated
258                                          The IgG3 subclass response was higher in AF fractions from D
259 h mean fluorescence intensity, rarely of the IgG3 subclass, and often capable of binding C1q.
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
262 s, and in vivo efficacies, with the IgG1 and IgG3 subclasses reacting similarly.
263 dies with strong complement-binding IgG1 and IgG3 subclasses.
264 sera is predominantly restricted to IgG1 and IgG3 subclasses.
265 properties compared with the IgG1, IgG2, 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 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
271 lations occurred, resulting in increased IgM/IgG3 titers to the oxidation-specific epitopes.
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
274 t in the IgG subclass profile from IgG2a and IgG3 to IgG1 in the sd-tg MRL-lpr mice.
275 d by combining an engineered hinge domain of IgG3 to increase Fab domain flexibility necessary for he
276             The age and tissue dependence of IgG3 transcription paralleled the developmental persiste
277  more pulmonary eosinophilia than IgG2a- and IgG3-treated C57BL/6J x 129/Sv mice.
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            We describe full-length IgG2b and IgG3 versions of JM4 that target the coreceptor-binding
282 with ~1 muM KD, whereas the interaction with IgG3 was a magnitude weaker.
283                                              IgG3 was an efficient opsonin for C. neoformans in Fcgam
284 y, while production of cat-specific IgG1 and IgG3 was not stimulated by MAT-Feld1 ILIT.
285                        No binding to IgG1 or IgG3 was observed.
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 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.
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

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