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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.
7 g both the signal-transducing gamma-chain of IgG receptors and SHIP or Ig and SHIP produce less IL-6.
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
13 lation was blocked by TrkC-IgG (but not TrkB-IgG) receptor bodies, further suggesting that GM1 activa
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
20 ripts that encode Mac-2 and the low-affinity IgG receptors Fc-gamma RIIb2, Fc-gamma RIII, and the FcR
23 ase (eNOS) through processes mediated by the IgG receptor Fcgamma receptor IIB (FcgammaRIIB), its imm
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
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
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
45 utable to anti-Abeta antibody stimulation of IgG receptor (FcR)-mediated phagocytic clearance of Abet
47 blocking mAbs specific for these activating IgG receptors have enabled, for the first time, the inve
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
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
58 ted phagocytosis through all ITAM-containing IgG receptors using a molecular mechanism distinct from
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