ライフサイエンスコーパス: IgG receptor

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 f Ag, which led to downmodulation of surface IgG receptors and triggered their activation.

9 on and activation of both CD32 (low affinity IgG receptor) and alphaMss2 integrin.

10 e with NSAID-LTP-A of the IFN-gamma pathway, IgG receptors, and ADORA3 might provide the pathogenic b

11 ntestinal eosinophils expressed low-affinity IgG receptors, and the activating receptor FcgammaRIII w

12 ssociated with a variable human milk IgA and IgG receptor-binding domain-specific antibody response o

13 inity, whereas FcgammaRIIa, the low-affinity IgG receptor, binds CRP with high affinity.

14 FcgammaRIa, the high-affinity IgG receptor, binds CRP with low affinity, whereas Fcgam

15 lation was blocked by TrkC-IgG (but not TrkB-IgG) receptor bodies, further suggesting that GM1 activa

16 Ag retention in the lungs did not rely on IgG receptors, C1q, neutrophils, or macrophages.

17 ells or by cross-linking of the low-affinity IgG receptor, CD16, by Ag-Ab immune complexes.

18 t relies on engineered overexpression of the IgG receptor CD64.

19 Increased expression of the IgG receptor (CD64) in patients with LTP-A was mirrored

20 re employed to determine the contribution of IgG receptors, complement component C1q, myeloid cell ty

21 sibility is that aggregation of low affinity IgG receptors could signal mast cells to adhere to compo

22 ng IgG-allergen immune complexes that induce IgG receptor-expressing neutrophils and monocytes/macrop

23 n mast cells might express the high-affinity IgG receptor Fc gamma RI and in turn be activated throug

24 thin the cytoplasmic domain of the leukocyte IgG receptor Fc gamma RIIA that affects the amplitude of

25 ss-linking of Fc epsilonRI to the inhibitory IgG receptor Fc gammaRIIb.

26 ripts that encode Mac-2 and the low-affinity IgG receptors Fc-gamma RIIb2, Fc-gamma RIII, and the FcR

27 However, because IgG receptors (Fc-gamma RIIb2, Fc-gamma RII) were presen

28 elet activation by the platelet low-affinity IgG receptor, Fc gamma RIIA.

29 SAP activates the high-affinity IgG receptor Fcgamma receptor I (FcgammaRI; CD64) and th

30 ase (eNOS) through processes mediated by the IgG receptor Fcgamma receptor IIB (FcgammaRIIB), its imm

31 The CD32a immunoglobulin G (IgG) receptor (Fcgamma receptor IIa) is a potential ther

32 IgG receptors (FcgammaR) were also found on mouse basoph

33 gG antibodies that signal via the inhibitory IgG receptor, FcgammaR2b, suppressing both immediate all

34 of CD11b and instead required the activating IgG receptor FcgammaRI (CD64) both in vitro and during c

35 w that expression of CD64, the high-affinity IgG receptor FcgammaRI, distinguishes conventional DCs f

36 ons (Shc, Grb2, and Cbl) after high affinity IgG receptor (FcgammaRI) cross-linking, leading to the f

37 The high-affinity IgG receptor, FcgammaRI (CD64), is constitutively expres

38 The sole high-affinity IgG receptor, FcgammaRI plays a significant role in immu

39 regating these receptors to the low affinity IgG receptor FcgammaRII.

40 A high level of low affinity IgG receptor (FcgammaRII, CD32), but no expression of Fc

41 ons, in particular those of human activating IgG receptor FcgammaRIIA (CD32A).

42 s (ICs) activated platelets in vitro via the IgG receptor (FcgammaRIIa).

43 signal transduction by the human-restricted IgG receptor, FcgammaRIIa.

44 IgG-opsonized pathogens by the low-affinity IgG receptor FcgammaRIIB in a "zipper-like" manner and a

45 Here, we have shown that activation of the IgG receptor FcgammaRIIB in endothelium by hyposialylate

46 s a counterbalance, the coaggregation of the IgG receptor FcgammaRIIB mediates inhibitory signals via

47 A requirement for the IgG receptor FcgammaRIIB was demonstrated in vitro using

48 eficient in the inhibitory immunoglobulin G (IgG) receptor FcgammaRIIB are protected from obesity-ind

49 Conversely, mRNA for the low-affinity IgG receptor (FcgammaRIIB), implicated in negative regul

50 ed upon co-clustering of sIg with the B cell IgG receptor, FcgammaRIIb.

51 in this model is mediated by the activating IgG receptor FcgammaRIII, we pre-incubated bone marrow-d

52 predominant contribution of mouse activating IgG receptors FcgammaRIII and FcgammaRIV to models of au

53 tive systemic anaphylaxis depends on IgG and IgG receptors (FcgammaRIIIA and FcgammaRIV) expressed by

54 s were directly captured by KCs via multiple IgG receptors FcgammaRs, whereas IgM-opsonized bacteria

55 mation and anaphylaxis through engagement of IgG receptors (FcgammaRs) in FcgammaR-humanized mice.

56 Stimulatory IgG receptors (FcgammaRs) on bone marrow-derived cells c

57 utable to anti-Abeta antibody stimulation of IgG receptor (FcR)-mediated phagocytic clearance of Abet

58 therapeutic inhibitors of complement and the IgG receptor FcRn, a testament to our improved comprehen

59 and FcgammaRIIa as the two main responsible IgG receptors for the breaking of immune tolerance of mi

60 The in vivo roles of IgG receptors have been addressed using specific FcR kno

61 blocking mAbs specific for these activating IgG receptors have enabled, for the first time, the inve

62 mmaRI that confirm the role of high-affinity IgG receptors in vivo.

63 mouse strain in which the human low-affinity IgG receptor locus, comprising both activating (hFcgamma

64 mAbs lacking the capacity to activate mouse IgG receptors not only failed to induce anaphylaxis or t

65 ient peritoneal macrophages show evidence of IgG receptor stimulation.

66 nRII, whereas constitutive expression of the IgG receptor subtype, FcgammaRIII, was unaltered.

67 ess involves the FcgammaRIIB, a low-affinity IgG receptor that is expressed on B cells and acts as a

68 motif-containing 21 (TRIM21) is a cytosolic IgG receptor that mediates intracellular virus neutraliz

69 or (FcyR) IIa and FcyRIII as the two primary IgG receptors that are responsible for the induction of

70 hil phagocytosis proceeds from the clustered IgG receptor to Src to phosphatidylinositol 3-kinase and

71 h peripheral macrophages, responding through IgG receptors to secreted IgG, produce IL-6, to support

72 tein-12 (also known as TYROBP) interactions, IgG receptor-triggered events, immunoregulation, and IL-

73 Fc gamma RIIa is a low affinity IgG receptor uniquely expressed in human cells that prom

74 ted phagocytosis through all ITAM-containing IgG receptors using a molecular mechanism distinct from