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1 in-10 (IL-10) and FcgammaRIII (an activating IgG receptor).
2 ion is negatively regulated by an inhibitory IgG-receptor.
3 A) and inhibitory (FcgammaRIIB) low-affinity IgG receptors.
4 eosinophils could be triggered through their IgG receptors.
5 e mice by using histamine, as well as IgE or IgG receptor aggregation.
6 t neither alone) or by a combination of anti-IgG receptor and anti-IgE antibodies.
7 g both the signal-transducing gamma-chain of IgG receptors and SHIP or Ig and SHIP produce less IL-6.
8 on and activation of both CD32 (low affinity IgG receptor) and alphaMss2 integrin.
9 e with NSAID-LTP-A of the IFN-gamma pathway, IgG receptors, and ADORA3 might provide the pathogenic b
10 ntestinal eosinophils expressed low-affinity IgG receptors, and the activating receptor FcgammaRIII w
11 inity, whereas FcgammaRIIa, the low-affinity IgG receptor, binds CRP with high affinity.
12                FcgammaRIa, the high-affinity IgG receptor, binds CRP with low affinity, whereas Fcgam
13 lation was blocked by TrkC-IgG (but not TrkB-IgG) receptor bodies, further suggesting that GM1 activa
14 ells or by cross-linking of the low-affinity IgG receptor, CD16, by Ag-Ab immune complexes.
15                  Increased expression of the IgG receptor (CD64) in patients with LTP-A was mirrored
16 sibility is that aggregation of low affinity IgG receptors could signal mast cells to adhere to compo
17 n mast cells might express the high-affinity IgG receptor Fc gamma RI and in turn be activated throug
18 thin the cytoplasmic domain of the leukocyte IgG receptor Fc gamma RIIA that affects the amplitude of
19 ss-linking of Fc epsilonRI to the inhibitory IgG receptor Fc gammaRIIb.
20 ripts that encode Mac-2 and the low-affinity IgG receptors Fc-gamma RIIb2, Fc-gamma RIII, and the FcR
21                             However, because IgG receptors (Fc-gamma RIIb2, Fc-gamma RII) were presen
22 elet activation by the platelet low-affinity IgG receptor, Fc gamma RIIA.
23 ase (eNOS) through processes mediated by the IgG receptor Fcgamma receptor IIB (FcgammaRIIB), its imm
24                  The CD32a immunoglobulin G (IgG) receptor (Fcgamma receptor IIa) is a potential ther
25                                              IgG receptors (FcgammaR) were also found on mouse basoph
26 of CD11b and instead required the activating IgG receptor FcgammaRI (CD64) both in vitro and during c
27 w that expression of CD64, the high-affinity IgG receptor FcgammaRI, distinguishes conventional DCs f
28 ons (Shc, Grb2, and Cbl) after high affinity IgG receptor (FcgammaRI) cross-linking, leading to the f
29                            The high-affinity IgG receptor, FcgammaRI (CD64), is constitutively expres
30                       The sole high-affinity IgG receptor, FcgammaRI plays a significant role in immu
31 regating these receptors to the low affinity IgG receptor FcgammaRII.
32                 A high level of low affinity IgG receptor (FcgammaRII, CD32), but no expression of Fc
33 ons, in particular those of human activating IgG receptor FcgammaRIIA (CD32A).
34 s (ICs) activated platelets in vitro via the IgG receptor (FcgammaRIIa).
35  signal transduction by the human-restricted IgG receptor, FcgammaRIIa.
36   Here, we have shown that activation of the IgG receptor FcgammaRIIB in endothelium by hyposialylate
37 s a counterbalance, the coaggregation of the IgG receptor FcgammaRIIB mediates inhibitory signals via
38                        A requirement for the IgG receptor FcgammaRIIB was demonstrated in vitro using
39        Conversely, mRNA for the low-affinity IgG receptor (FcgammaRIIB), implicated in negative regul
40 ed upon co-clustering of sIg with the B cell IgG receptor, FcgammaRIIb.
41  in this model is mediated by the activating IgG receptor FcgammaRIII, we pre-incubated bone marrow-d
42 predominant contribution of mouse activating IgG receptors FcgammaRIII and FcgammaRIV to models of au
43 tive systemic anaphylaxis depends on IgG and IgG receptors (FcgammaRIIIA and FcgammaRIV) expressed by
44                                  Stimulatory IgG receptors (FcgammaRs) on bone marrow-derived cells c
45 utable to anti-Abeta antibody stimulation of IgG receptor (FcR)-mediated phagocytic clearance of Abet
46                         The in vivo roles of IgG receptors have been addressed using specific FcR kno
47  blocking mAbs specific for these activating IgG receptors have enabled, for the first time, the inve
48 mmaRI that confirm the role of high-affinity IgG receptors in vivo.
49 mouse strain in which the human low-affinity IgG receptor locus, comprising both activating (hFcgamma
50  mAbs lacking the capacity to activate mouse IgG receptors not only failed to induce anaphylaxis or t
51 ient peritoneal macrophages show evidence of IgG receptor stimulation.
52 nRII, whereas constitutive expression of the IgG receptor subtype, FcgammaRIII, was unaltered.
53 ess involves the FcgammaRIIB, a low-affinity IgG receptor that is expressed on B cells and acts as a
54  motif-containing 21 (TRIM21) is a cytosolic IgG receptor that mediates intracellular virus neutraliz
55 hil phagocytosis proceeds from the clustered IgG receptor to Src to phosphatidylinositol 3-kinase and
56 h peripheral macrophages, responding through IgG receptors to secreted IgG, produce IL-6, to support
57              Fc gamma RIIa is a low affinity IgG receptor uniquely expressed in human cells that prom
58 ted phagocytosis through all ITAM-containing IgG receptors using a molecular mechanism distinct from

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