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1 borate to 'stabilize' the ternary pathogenic immune complex.
2 on follicular dendritic cells in the form of immune complex.
3 ibodies through immunization with sialylated immune complexes.
4 rsistently infected mice specifically lacked immune complexes.
5 from that employed during the endocytosis of immune complexes.
6 ith synthetic TLR agonists or RNA-containing immune complexes.
7 uggested the development of antigen-antibody immune complexes.
8 he low-affinity IgG receptor, CD16, by Ag-Ab immune complexes.
9 d were highly efficient in taking up OVA/IgG immune complexes.
10 ous neutrophil stimulation with OVA/anti-OVA immune complexes.
11 of each clone to form dimeric and multimeric immune complexes.
12 nd increases levels of free Ag released from immune complexes.
13 eptor gammaII A, a low-affinity receptor for immune complexes.
14 the adaptive immune response, and removal of immune complexes.
15 h macrophages treated with Ft LVS-containing immune complexes.
16 aRIIa and FcgammaRIIb comparably bind dengue immune complexes.
17 on by either integrin ligands or immobilized immune complexes.
18 and are released as insoluble, amyloid-like immune complexes.
19 cgammaRs occurring in the form of multimeric immune complexes.
20 FcgammaR engagement using antigen-containing immune complexes.
21 ry effect on phagocytosis of immune-adherent immune complexes.
22 lar patterns such as IgG- and IgM-containing immune complexes.
23 and misfolded proteins, forming circulating immune complexes.
24 e uptake and cycling of complement-opsonized immune complexes.
25 culating autoantibodies and the formation of immune complexes.
26 rheumatoid-factor B cells by DNA-containing immune complexes.
27 IgG3, which self-associates to form large immune complexes, accounts for more than 97% of the mous
30 This study provides evidence that DENV-2 immune complexes activate Syk to mediate elevated expres
32 LF were also elevated in C5a-induced and IgG immune complex ALI models, suggesting a common inflammat
33 ation of BCR signaling in the absence of IgE immune complex and suggest that CD23 down-regulates BCR
34 (Horseradish Peroxidase) which binds to the immune complex and the response was observed using Hydro
35 features are not associated with circulating immune complexes and C3 deposition and are more pertinen
37 ts in brain with a corresponding increase in immune complexes and decrease in C3 concentration (by 60
38 fM analyte because beads attached via single-immune complexes and DNA strands form tethers, and tethe
39 iated through the interaction between RA IgG immune complexes and IgG Fc receptors on immune cells.
42 due to release of HCV-Ags sequestered in HCV immune complexes and should not be used in any HCV-Ags,
43 FcRn promotes the formation of subepithelial immune complexes and subsequent glomerular pathology lea
44 sh that SKAR is present in cap-binding CBP80 immune complexes and that this interaction is mediated b
45 ystemic lupus erythematosus, deposits of IgG-immune complexes and the activation of complement in the
46 ergens influenced the shape of the resulting immune complexes and the magnitude of effector cell acti
47 eveloping nephritis, despite the presence of immune complexes and the production of proinflammatory c
48 tructural elucidation of the nature of these immune complexes and their biological activity should pr
49 ory sites, where atherogenic factors such as immune complexes and/or pathogens can activate the endot
50 Isolated neutrophils were incubated with immune complexes, and activation and release of NETs wer
51 egates, diffuse parenchymal and perivascular immune complexes, and complement depositions were all pr
53 Human NK cells are activated by cytokines, immune complexes, and signals transduced via activating
55 GP patients had no circulating FH-containing immune complexes, and their anti-FH IgG had a weaker aff
57 gated antibody-dependent phagocytosis of HIV immune complexes, and we observed significant difference
58 te complement-tagged inflammatory particles (immune complexes, apoptotic/necrotic debris, and microbe
59 against anti-TNF-alpha Abs, suggesting that immune complexes are a major determinant of this immuniz
60 ting Fcgamma receptors (FcgammaRs) that bind immune complexes are controlled by a single inhibitory r
63 dentify specific target antigens in PAH lung immune complexes as a starting point toward resolving th
64 ross-reactivity for HT-2 and T-2 toxins, the immune complex assay is highly specific for HT-2 alone.
66 that epitope mutability and accessibility to immune complex assembly are important attributes to cons
67 e, in most patients with C3 glomerulopathies/immune complex-associated membranoproliferative glomerul
68 une responses as well as in the clearance of immune complexes, autoreactivity to complement component
69 mmatory Syk-ERK signaling axis requires DENV immune complexes, because DENV-2 in the presence of sero
73 via proinflammatory cytokines released upon immune complex binding to other FcgammaR-expressing inna
75 ively, have no influence on monomeric IgG or immune complex binding, but FcRgamma signaling is decrea
76 e extracellular domain of FcgammaRI, reduces immune-complex binding of FcgammaRI whereas monomeric Ig
77 of 10(4) molar excess of IgM or its soluble immune complexes, but it could be inhibited by addition
80 uptake of IgM and minimal endocytosis of IgG immune complexes by neutrophils was observed, in contras
81 vation threshold of innate effector cells to immune complexes by stimulating the up-regulation of the
82 vation threshold of innate effector cells to immune complexes by stimulating the upregulation of the
83 is study, we investigated how the size of an immune complex can affect the interaction of normal and
85 ion of idiopathic nephrotic syndrome with no immune complexes can improve the sensitivity to detect s
86 ation of the FcgammaR via antigen containing immune complexes can lead to the generation of reactive
89 rkedly impaired binding of huIgG1 and huIgG2 immune complexes compared with huFcgammaRIIa (His(131)).
90 We found that FDCs took up and retained self-immune complexes composed of ribonucleotide proteins, au
91 tiinfluenza antibodies by demonstrating that immune complexes composed of sialylated antihemagglutini
92 ake up and internalize donor cell-associated immune complexes composed of specific monoclonal antibod
93 RV144, pointed to mechanistic insights into immune complex composition that may underlie protective
94 se immunodeposits originate from circulating immune complexes consisting of anti-glycan antibodies bo
95 ntibodies specific for Fel d1 and exposed to immune complexes consisting of Fel d1-specific IgG antib
96 an autoimmune disease mediated by pathogenic immune complexes consisting of galactose-deficient IgA1
103 an autoimmune thrombotic disorder caused by immune complexes containing platelet factor 4 (PF4), ant
106 and suggest that high levels of pre-existing immune complexes could limit the effectiveness of antibo
107 with IgG, IgM, C1q, and C4d, consistent with immune complex dependent activation of the classical com
109 orly activate effector mechanisms, reveal an immune-complex-dependent, complement- and FcR-independen
111 glomerular capillaries are frequent sites of immune complex deposition and subsequent neutrophil accu
112 terized by autoantibody production and renal immune complex deposition leading to chronic glomerulone
115 ory cytokines and autoantibodies, glomerular immune complex deposition, and evidence of kidney damage
116 duction of antibodies to self-nucleic acids, immune complex deposition, and tissue inflammation such
117 l nerve antigens, but additionally encompass immune complex deposition, cellular infiltration, and cy
119 er from hypersensitivity mechanisms, or from immune-complex deposition via anti-adalimumab antibodies
120 elected scFv was applied in serodiagnosis by immune complexes detection in serum samples from individ
125 organisms to FcR in mice i.n., with MAb-iFT immune complexes, enhances F. tularensis-specific immune
126 an renal disease has long been recognized in immune-complex excess syndromes such as systemic lupus e
127 way Treg responses; boosting Tregs with IL-2 immune complexes failed to restore normal levels of Treg
128 although both isoforms similarly bind dengue-immune complexes, FcgammaRIIa efficiently internalized v
130 e that in contrast to internalization of IgG immune complexes, FcgammaRIIb-augmented internalization
132 f the AP in CAIA through binding to sites of immune complex formation and complement activation.
134 s on Fcgamma receptor and the requirement of immune complex formation for effector cell activations.
135 ximal tubule antigen-specific antibodies and immune complex formation has not been well characterized
136 In this article, we provide evidence that immune complex formation of serum IgA plays an important
139 ata provide a mechanism explaining increased immune-complex formation and disease exacerbation during
140 er characterized by autoantibody production, immune-complex formation, and altered cytokine expressio
141 nd allows the calculation of the kinetics of immune complexes' formation in a continuous-flow system
143 ntified and confirmed as highly expressed in immune complexes from 16 hereditary and idiopathic PAH v
144 lar mechanism for the hand-over of CR3-bound immune complexes from macrophages to CR2-presenting cell
145 lammatory conditions, and they remove Ig and immune complexes from the glomerular basement membrane (
146 Herein, we show that increased amounts of immune complexes generated in mice persistently infected
148 mportant extrahepatic manifestations include immune complex glomerular disease, accelerated progressi
149 sults in increased systemic inflammation and immune complex glomerulonephritis, despite intact TLR si
151 rular C4d staining in 18 biopsy specimens of immune-complex GN, 30 biopsy specimens of C3 GN, and 13
152 types, each with specific disease entities: immune-complex GN, pauci-immune GN, antiglomerular basem
153 of the immunoassay was introduced by an anti-immune complex (IC) antibody binding the primary antibod
154 A role for FcgammaRIIIa activation from immune complex (IC) ligation and sublytic terminal compl
156 ental effects of neutrophils using models of immune complex (IC)-mediated inflammation in mice immuno
157 se (EndoS) induced a dominant suppression of immune complex (IC)-mediated inflammation, such as arthr
158 ing several pathologic conditions, including immune complex (IC)-mediated inflammatory/autoimmune dis
162 e of phagocytic cells binds complement-bound immune complexes (IC), playing an important role in the
163 transgenic mice with IgG2a(a) anti-chromatin immune complexes (ICs) activated RF B cells in a BCR- an
164 dies demonstrated that allergen-specific IgG immune complexes (ICs) and house dust mite (HDM) extract
166 ion is complexed to Abs, and these resulting immune complexes (ICs) are a prominent feature of chroni
168 riven immune responses that are modulated by immune complexes (ICs) are known to inhibit IFN-gamma-de
169 ose EVs are responsible for the formation of immune complexes (ICs) containing anti-MASP SP IgGs in p
171 e found that FDCs acquired complement-coated immune complexes (ICs) from noncognate B cells via compl
175 therapeutic target for diseases in which IgG immune complexes (ICs) mediate inflammation, such as hep
177 demonstrate that FcgammaR engagement by IgG immune complexes (ICs) stimulates DC migration from peri
178 dary exposure of the immune system to an Ag, immune complexes (ICs) that contain the unprocessed Ag a
180 the mAb had formed immunogenicity-enhancing immune complexes (ICs) with nucleosomal Ags during cell
181 In this study, we identify a role for IgG-immune complexes (ICs), FcgammaRs, and BAFF during the f
182 dividuals and stimulated with RNA-containing immune complexes (ICs), herpes simplex virus (HSV) or th
186 ansfer and uptake of allergen-containing IgG immune complexes (Ig-ICs) by gut dendritic cells (DCs).
187 t fragments with minimal or no deposition of immune complexes/Ig; the C3 is derived from activation o
188 ted GN results from glomerular deposition of immune-complexes/Ig and C3; the C3 is derived from activ
190 )-dependent transfer of maternal IgG and OVA immune complexes (IgG-IC) via breast milk and induction
191 egrade apoptotic debris contained within IgG-immune complexes (IgG-ICs) and promotes recycling and th
192 ll controversial; however, a receptor of IgG-immune complexes (IgG-ICs), FcgammaRIII, has been shown
193 mbers by administration of IL-2/anti-IL-2 Ab immune complexes (IL2C) or by adoptive transfer of ex vi
196 dy the functionality and distribution of the immune complex in the nitrocellulose membrane slides.
198 n can take place directly on IgA1-containing immune complexes in circulation and/or after their depos
199 o tissue damage, we investigated whether IgA immune complexes in plasma and synovial fluid of RA pati
200 ough deposition of immunoglobulin-containing immune complexes in premalignant tissue and Fcgamma rece
201 on glomerular podocytes and form deposits of immune complexes in situ in the glomerular capillary wal
205 ects the trapping of anti-H1N1 antibodies in immune complexes in the lungs, associated with poor spec
207 psilonRII-mediated signaling by allergen-IgE immune complexes increased IFN-gamma production in B cel
211 r autoimmune arthritis and thrombocytopenia, immune complex-induced airway inflammation, and active a
217 " Taking into account that the deposition of immune complexes is a major event in acute inflammation
218 une activation via clearance of inflammatory immune complexes, it is also plausible that Fc receptor
219 Decrease in C3 could alter the transport of immune complexes leading to an increase in IgG deposits
220 d: large scroll-like immunotactoid deposits, immune complex-like deposits, and randomly arranged fibr
221 of-principle, immune sandwich assay in which immune complexes link micron-size beads via DNA tethers
222 ssays applied for detection of GAD65 and its immune complexes may thus enable improved diagnosis and
224 and 55 (CD46 and CD55) regulate circulating immune complex-mediated complement activation in idiopat
225 n CD20-expressing tumors, as well as reduced immune complex-mediated cross-presentation to T cells.
229 h FLIPr-like prevented the development of an immune complex-mediated FcgammaR-dependent Arthus reacti
230 gated the role of FcRn in the development of immune complex-mediated glomerular disease in mice.
232 uced higher anti-dsDNA IgG Abs and developed immune complex-mediated glomerulonephritis, compared wit
235 mmarize, C4d serves as a positive marker for immune complex-mediated GN but is absent or minimally de
240 plement-mediated C3 glomerulopathy (C3G) and immune complex-mediated membranoproliferative GN (IC-MPG
242 nts with pathology-confirmed complement- and immune complex-mediated MPGN who had available ophthalmo
244 mportant role for BTK in the pathogenesis of immune complex-mediated nephritis, and BTK inhibition as
247 t glomerulopathy after rigorous exclusion of immune complexes of other cause, particularly recurrent
249 Ib) that, upon multivalent binding of IgG in immune complexes or on opsonized targets, mediate respon
251 plement and FcR independent and results from immune complex precipitation in glomerular capillaries,
252 esolution structure of a type III RNA-guided immune complex provides new insights into the mechanisms
254 macrophages detect and scavenge circulating immune complexes "pumped" into the interstitium via tran
255 lasts to directly interact with autoantibody immune complexes, rather than being influenced indirectl
256 n of the antigen via formation of aggregated immune complexes, reduction of bacterial infectivity, ma
259 Additionally, in vitro stimulation with immune complexes resulted in significantly less CXCL-1 a
261 n addition, native MS analysis of bsAb/JAM-A immune complexes revealed that bsAb can bind up to two a
263 suggesting they are mediated by PGN-anti-PGN immune complexes signaling through Fcgamma receptor IIa.
264 Strikingly, we found that stimulation with immune complexes significantly upregulated the expressio
266 s brought about by FcgammaRI engagement with immune complexes such as the inhibition of IFNgamma and
267 clinical/serological phenotypes mediated by immune complexes, such as peripheral neuropathy, vasculi
270 oduction, induced by nucleic-acid-containing immune complexes that activate endosomal Toll-like recep
271 ism for trans-endothelial transport of small immune complexes that activate strategically positioned
272 reover, the autoantibodies they produce form immune complexes that can activate myeloid cells and the
273 inhibition of the formation of nephritogenic immune complexes that could be used as a disease-specifi
274 IgAN develop characteristic IgA1-containing immune complexes that deposit in the glomerular mesangiu
277 ination of direct platelet activation by HIT immune complexes through FcgammaRIIA and transactivation
278 s the transport and delivery of bacteria and immune complexes to phagocytes, through a process known
283 e, FcgammaRIIB was required for Sendai virus immune complex uptake by splenic pDCs in vitro, and inte
285 ding of dimeric rsFcgammaR ectodomains to Ab immune complexes was affected by Ab subclass, presentati
286 rmed that the rapid clearance of these large immune complexes was associated with Fcgamma receptor-de
287 nd Y1 RNA complexed with SLE patient Abs and immune complexes was measured in a cross-section of 228
288 ated Francisella tularensis (iFt)-containing immune complexes, we observed a significant increase in
292 RF isotypes were measured with ELISA, and immune complexes were precipitated using polyethylene gl
293 es, and degranulation induced by immobilized immune complexes, were reduced in Ptpn22(-/-) neutrophil
294 hese autoantibodies trigger the formation of immune complexes, which are hypothesized to cause enhanc
296 erum protein TXNDC16 is bound in circulating immune complexes, which were found both in meningioma an
297 is mediated through the interaction of viral immune complexes with FcgammaRs, with notable efficiency
299 te more effective target functions to design immune complexes with improved biological functions.
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