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1 with known concentrations for human IgE and IgG4 .
2 mulate somatic mutation of allergen-specific IgG4.
3 a significant increase in allergen-specific IgG4.
4 flammatory and blocking antibody function of IgG4.
5 , AIT is often associated with production of IgG4.
6 ligands without steric clashes, unlike human IgG4.
7 ted to the accumulation of anti-inflammatory IgG4.
8 IgG3 against the antigen panel and anti-C1q IgG4.
9 In these regards, it resembles human IgG4.
10 otal IgE, specific IgE, and Der p 1-specific IgG4.
11 nds favor half-molecule exchange in vivo for IgG4.
12 s tetrameric human hemoglobin (Hb) and human IgG4.
13 compared to those with anti-neurofascin-155 IgG4.
14 per high-power field that were positive for IgG4.
16 We found an association between levels of IgG4 above the upper reference limit and specific HLA ha
19 ng, along with observed granular deposits of IgG4, abundant IgG4-containing plasma cells, and serum l
21 is demonstrated for the first time how anti-IgG4 affinity chromatography can be used to prepare phys
22 ot nonallergic subjects, are able to produce IgG4 after cognate interactions with sTH2 clones and Fel
24 LIT were assayed using ImmunoCAP for IgE and IgG4 against whole peanut, Ara h 1, Ara h 2, Ara h 3, Ar
31 ncentrations of allergen-specific IgE, IgG1, IgG4 and IgA to seven Bet v 1-related food allergens wer
34 inity IgG1 and IgG3, and 1 had high-affinity IgG4 and later developed low-titer FVIII inhibitors.
35 ines to skew the immune response from IgE to IgG4 and regulation of dendritic cell, mast cell, basoph
37 d (iii) their capacity to produce inhibitory IgG4 and sialylated IgG able to mediate anti-inflammator
39 APT), skin testing, serum levels of specific IgG4 and specific IgE and safety were also evaluated.
40 detection of food allergen-specific IgE and IgG4 , and compared it with ImmunoCAP and ImmunoCAP ISAC
45 -specific IgG, and casein-specific IgE, IgG, IgG4, and IgM levels, as well as immunoglobulin free lig
46 fore might affect the serum concentration of IgG4, and increased IgG4 might be a marker of a distinct
47 t some of the biological properties of human IgG4, and review the recent crystal structures of IgG4-F
48 r, HLA-B*08, than patients without increased IgG4, and significantly higher frequencies of HLA-B*07 a
58 py results in the production of blocking IgG/IgG4 antibodies that can inhibit IgE-dependent activatio
59 ver, children with transient CMA had IgE and IgG4 antibodies that more often recognized the same epit
61 nd measurements of allergen-specific IgE and IgG4 antibodies were performed before and after treatmen
65 ecently, a human monoclonal Phl p 7-specific IgG4 antibody (mAb102.1F10) was isolated from a patient
66 aimed to investigate differences in IgE and IgG4 antibody binding to CM epitopes between patients wi
70 rienced B cells with the capacity to produce IgG4 are present in allergic subjects and (2) cat allerg
71 0(-)CD38(hi) plasmablasts, which are largely IgG4(+), are increased in patients with active IgG4-RD.
73 simultaneous detection of allergen-specific IgG4 , as a potential parameter for tolerance developmen
74 uencing accurately distinguish patients with IgG4-associated cholangitis/autoimmune pancreatitis (n =
75 ry T-cell (Treg) cytokines in IgG4-RD and in IgG4-associated MZL and IgG4-negative MZL using real-tim
77 it differs between ocular adnexal MZLs with (IgG4-associated MZL) and without (IgG4-negative MZL) num
78 ckground in IgG4-negative MZLs suggests that IgG4-associated MZLs may have a different pathogenesis.
80 idiopathic membranous nephropathy (IMN) have IgG4 autoantibodies against phospholipase A2 receptor (P
83 g plays a substantial role in triggering the IgG4 autoantibody development in FS and provide new insi
85 fogo selvagem [FS]) in which the pathogenic IgG4 autoantibody response to the self-antigen desmoglei
87 c gating strategy to reliably identify blood IgG4(+) B cells to study their cellular and molecular ch
90 r intensity and broader diversity of IgE and IgG4 binding have been found in children with persistent
91 time of tolerance development, both IgE and IgG4 binding intensity decreased significantly, particul
92 Interestingly, differences between IgE and IgG4 binding intensity to CM peptides decreased when the
95 has a half-life as long as that of IgG2 and IgG4, binds the FcgammaR receptor, and activates complem
96 veloped IMN with intense staining for PLA2R, IgG4, C3, C5b-9, factor B, and properdin and very weak s
98 ange in allergen-specific immunoglobulin G4 (IgG4), change in asthma control or asthma quality-of-lif
103 observed granular deposits of IgG4, abundant IgG4-containing plasma cells, and serum levels of IgG4 r
105 glycoforms of IgG 2/3, and 19 glycoforms of IgG4) directly in unfractionated samples of human plasma
109 ers and chemokine receptors was performed on IgG4-expressing B cells, and IgG4 transcripts were analy
112 x conditions, the S228P mutation can prevent IgG4 FAE to undetectable levels both in vitro and in viv
115 lytical ultracentrifugation showed that both IgG4 forms were principally monomeric with sedimentation
117 RT-PCR, we amplified, cloned, and sequenced IgG4 H chain transcripts of PBMCs from 10 children with
122 zed that component-resolved analysis of IgE, IgG4, IgA, IgA1, and IgA2 may identify potential biomark
127 Increases in peanut-specific IgG4 levels and IgG4/IgE ratios were observed in peanut EPIT-treated par
128 e dust mite-specific IgG/IgE ratios (but not IgG4/IgE ratios) were significantly lower in children wi
131 = 0.038), IgE-OVM (P = 0.032), and a higher IgG4/IgE-OVM ratio (P = 0.013) were associated with clin
134 chain reaction (qPCR) protocol analyzing the IgG4/IgG RNA ratio in blood also achieves excellent diag
136 propose a new diagnostic algorithm based on IgG4/IgG1 ratio that may be used in clinical practice to
137 ymptoms, total and allergen-specific IgE and IgG4, immune function, and inflammatory markers were obt
139 and casein-specific IgG and casein-specific IgG4 in patients with CM-FPIES versus those tolerating C
140 gths that were even weaker for IgG3 than for IgG4 in the case of allotype G3m(c3c5*/6,24*), whereas G
143 , the specific T-cell response that leads to IgG4 induction during chronic allergen exposure remains
144 ific IgG1 promote OPA, and that CSP-specific IgG4 interferes with OPA, which we subsequently confirme
147 ely devoid of effector function, whereas the IgG4 isotype can undergo in vivo Fab arm exchange leadin
148 by IgG1 and IgG3, whereas the Th2-associated IgG4 isotype was only detected at very low amounts.
158 immunotherapy-induced grass pollen-specific IgG4 levels decreased to near pre-immunotherapy levels a
159 in allergen component-specific serum IgE and IgG4 levels during the updosing phase of subcutaneous im
160 , this qPCR test performed better than serum IgG4 levels in sensitivity (94% vs. 86%) and specificity
163 ped desensitization had a larger increase in IgG4 levels to alpha-lactalbumin (P = 0.034), beta-lacto
166 kin test results and peanut-specific IgE and IgG4 levels were found, with overall greater effects wit
168 ant differences in allergen-specific IgE and IgG4 levels, cytokine production by PBMCs, or basophil a
170 ta collected for a pharmaceutically relevant IgG4 mAb being characterized to determine the effects of
176 e serum concentration of IgG4, and increased IgG4 might be a marker of a distinct phenotype of PSC.
177 lts suggest that the overlap between IgE and IgG4 might be important in natural tolerance acquisition
178 c-Fc interactions are compatible with intact IgG4 molecules and may provide a model for the formation
179 ers to monitor and quantify FAE of their own IgG4 molecules in physiologically relevant matrices.
181 cterize biopharmaceutical samples, including IgG4 monoclonal antibodies (mAbs) and recombinant human
183 mab (CAT-354) is an IL-13-neutralising human IgG4 monoclonal antibody that has shown clinical benefit
184 ized serine 228 to proline (S228P) anti-IL-6 IgG4 mutant, it is demonstrated for the first time how a
185 y included skin test, serum specific IgE and IgG4, nasal allergen provocation test (NAPT), and advers
187 es in IgG4-RD and in IgG4-associated MZL and IgG4-negative MZL using real-time polymerase chain react
188 MZLs with (IgG4-associated MZL) and without (IgG4-negative MZL) numerous IgG4(+) plasma cells are unk
189 ce of a different inflammatory background in IgG4-negative MZLs suggests that IgG4-associated MZLs ma
190 nd increased or reduced levels of IgE, IgG1, IgG4 or IgA specific to most Bet v 1-related allergens.
193 sed the activity of nivolumab, a fully human IgG4 PD-1 immune checkpoint inhibitor antibody, for pati
199 Panelists agreed that a maximum number of 30 IgG4-positive plasma cells per high-power field in the o
200 The presence of oligoclonally restricted IgG4-positive plasma cells within inflammatory meningeal
201 -RHP are a lymphoplasmacytic infiltration of IgG4-positive plasma cells, storiform fibrosis, and obli
202 s expressed by the podocyte, and both induce IgG4-predominant humoral immune responses that produce c
203 and B-cell responses, regulation of IgE and IgG4 production, and inhibition of responses from eosino
205 icacy and safety of nivolumab, a fully human IgG4 programmed death 1 (PD-1) immune-checkpoint-inhibit
207 IgG-subclasses (sIgG1, sIgG4 including SIgE/IgG4 ratio), (iii) Serum inhibitory activity for IgE (Ig
209 h2 and regulatory T-cell (Treg) cytokines in IgG4-RD and in IgG4-associated MZL and IgG4-negative MZL
212 in tissue are hallmarks of the disease, and IgG4-RD is associated with increased IgG4 serum levels.
213 d IgE, suggesting that processes inherent to IgG4-RD itself rather than atopy per se contribute to th
222 Immunoglobulin G4 (IgG4)-related disease (IgG4-RD) of the biliary tree and pancreas is difficult t
223 xteen patients with histologically confirmed IgG4-RD, 11 patients with sarcoidosis, and 30 healthy su
225 phocyte signature" observed in patients with IgG4-RD, could support diagnosis and treatment monitorin
234 containing plasma cells, and serum levels of IgG4 reactive to specific foods, indicate that, in adult
236 ormed, and a diagnosis of immunoglobulin G4 (IgG4)-related disease was made based on identification o
241 The three central pathology features of IgG4-related disease are lymphoplasmacytic infiltration,
245 and effects from prednisone treatment among IgG4-related disease with salivary gland lesions (RD-SG)
246 rgans, is considered part of the spectrum of IgG4-related disease, and often arises in patients with
257 vels after therapy were linked to a specific IgG4 response, and production of blocking antibodies cor
259 und significant differences in IgE, IgG, and IgG4 responses between both active groups and the placeb
261 ignificantly decreased and allergen-specific IgG4 responses were significantly elevated (P < 0.001).
262 ular, hallmark histopathological features of IgG4-RHP are a lymphoplasmacytic infiltration of IgG4-po
270 properties compared with the IgG2, IgG3, and IgG4 subclasses and is the most exploited subclass in th
274 nezumab is a humanized anti-Abeta monoclonal IgG4 that binds multiple forms of Abeta, with higher aff
275 e a model for the formation of aggregates of IgG4 that can cause disease pathology in the absence of
276 ic esophagitis had increased serum levels of IgG4 that reacted with milk, wheat, egg, and nuts-the 4
278 ell frequency, cat allergen-specific IgE and IgG4 titers, and clinical status in adults with cat alle
280 after OIT regarding serum levels of IgE and IgG4 to milk and five milk allergen components evaluated
286 as performed on IgG4-expressing B cells, and IgG4 transcripts were analyzed for somatic hypermutation
287 hieving SU, subjects achieving SU had higher IgG4 values (P = .001) and lower egg skin prick test sco
290 ique non-IgG2 anti-DNA deposit, and anti-C1q IgG4 was mainly detected in subepithelial membranous dep
291 s: rLinB-13 was the top performing molecule; IgG4 was the most predominant antibody subclass and anti
296 tracellular proteins targeted by human serum IgG4 were identified by means of immunoblotting to scree
298 ith serum concentrations of Ves v 5-specific IgG4 which rose during AIT but almost reached pretreatme
300 reactivity in RA was against pepsin-cleaved IgG4, with a 35% prevalence, >/=5.8-fold higher than in
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