ライフサイエンスコーパス: complement-dependent cytotoxicity

1 antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity.

2 ment component C1q, and inability to mediate complement-dependent cytotoxicity.

3 nificant enhancement of daratumumab-mediated complement-dependent cytotoxicity.

4 antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity.

5 d the surface of carcinoma cells and induced complement-dependent cytotoxicity.

6 Treg are resistant to alemtuzumab-mediated, complement-dependent cytotoxicity.

7 iated Ab-dependent cellular cytotoxicity, or complement-dependent cytotoxicity.

8 ntibody-dependent cellular phagocytosis, and complement-dependent cytotoxicity.

9 CD20 molecules and impair rituximab-mediated complement-dependent cytotoxicity.

10 to identify inhibitors of NMO-IgG-dependent, complement-dependent cytotoxicity.

11 otoxicity compared with veltuzumab but lacks complement-dependent cytotoxicity.

12 pendent cellular toxicity, neither displayed complement-dependent cytotoxicity.

13 NK cell death occurs via both antibody- and complement-dependent cytotoxicity.

14 a strong negative impact on C1q binding and complement-dependent cytotoxicity.

15 athogens by mediating antibody-dependent and complement-dependent cytotoxicity.

16 When screened by complement-dependent cytotoxicity, 46% of the patients w

17 mechanisms to delete target cells, including complement-dependent cytotoxicity, Ab-dependent cellular

18 ation of tumor cell signaling, activation of complement-dependent cytotoxicity, Ab-dependent cellular

19 antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity activities of the anti

20 Ab-dependent cell-mediated cytotoxicity and complement-dependent cytotoxicity activities.

21 Ab-dependent cell-mediated cytotoxicity and complement-dependent cytotoxicity activities.

22 ral blood mononuclear cells, and had minimal complement-dependent cytotoxicity activity similar to th

23 A complete loss of complement-dependent cytotoxicity activity was seen with

24 lt in a dramatic increase in C1q binding and complement-dependent cytotoxicity activity.

25 ts exhibiting an increase in C1q binding and complement-dependent cytotoxicity activity.

26 addition, a GD3 antibody is shown to induce complement-dependent cytotoxicity against cells expressi

27 ntibody-dependent cellular cytotoxicity, and complement-dependent cytotoxicity against primary CLL ce

28 t significantly increased rituximab-mediated complement-dependent cytotoxicity against primary tumor

29 , an SSEA-4-specific mAb was found to induce complement-dependent cytotoxicity against SSEA-4(hi) GBM

30 ts with positive antihuman globulin-enhanced complement dependent cytotoxicity (AHG-CDC) crossmatches

31 -titer positive antihuman globulin-enhanced, complement-dependent cytotoxicity (AHG-CDC) cross-matche

32 phocyte cytotoxicity (antiglobulin-enhanced, complement-dependent cytotoxicity [AHG-CDC]) or assays (

33 It was shown that complement-dependent cytotoxicity and Ab-dependent cellu

34 cells are less susceptible to mATG-mediated complement-dependent cytotoxicity and ADCC.

35 Preclinical data suggest improved complement-dependent cytotoxicity and antibody-dependent

36 prostate cancer cell death, it also mediates complement-dependent cytotoxicity and antibody-dependent

37 IgG into F(ab')2 and Fc fragments inhibiting complement-dependent cytotoxicity and antibody-dependent

38 Rituximab mediates complement-dependent cytotoxicity and antibody-dependent

39 ined by positive results on SPA but negative complement-dependent cytotoxicity and flow cytometry cro

40 Circulating alloAb levels were quantified by complement-dependent cytotoxicity and flow cytometry.

41 ridge to HT had standard anti-human globulin complement-dependent cytotoxicity and retrospective flow

42 A class II alloantibodies (aAb) using direct complement-dependent cytotoxicity and several sensitive

43 to percent panel-reactive antibody (PRA; by complement-dependent cytotoxicity) and anti-MICA antibod

44 ng antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and antibody-dependen

45 tibody-dependent cell-mediated cytotoxicity, complement-dependent cytotoxicity, and antiinflammatory

46 ecognized GD2-positive tumor cells, mediated complement-dependent cytotoxicity, and exhibited protect

47 dy-dependent cellular cytotoxicity, mediates complement-dependent cytotoxicity, and induces apoptosis

48 ependent cell-mediated cytotoxicity, but not complement-dependent cytotoxicity, and inhibits prolifer

49 ecutive patients after exclusions yielded 94 complement-dependent cytotoxicity anti-human globulin cr

50 ages diverse mechanisms of action, including complement-dependent cytotoxicity, antibody-dependent ce

51 Complement-dependent cytotoxicity, antibody-dependent ce

52 ugh a variety of immune-mediated mechanisms (complement-dependent cytotoxicity, antibody-dependent ce

53 LL cells, we show that direct cell death and complement-dependent cytotoxicity are greatest with GA10

54 human IgG2 confer biological activity in the complement-dependent cytotoxicity assay in which the wil

55 The commonly performed complement-dependent cytotoxicity assay is insensitive c

56 e representative antibody-positive sera in a complement-dependent cytotoxicity assay with cultured me

57 ive antibody level, determined by use of the complement-dependent cytotoxicity assay, of 77+/-19% or

58 dy production was determined serially with a complement-dependent cytotoxicity assay.

59 Complement-dependent cytotoxicity assays were performed

60 detected by the PRA-STAT ELISA system and by complement-dependent cytotoxicity assays.

61 both Ab-dependent cellular cytotoxicity and complement-dependent cytotoxicity assays.

62 The blockers did not affect complement-dependent cytotoxicity caused by anti-GD3 ant

63 More than 2,000 complement dependent cytotoxicity (CDC) and 200 flow cro

64 C were related to loss in drug potency via a complement dependent cytotoxicity (CDC) bioassay.

65 In this study, we sought to test the role of complement dependent cytotoxicity (CDC) immune effector

66 n proposed that IgG may confer resistance to complement dependent cytotoxicity (CDC), a conventional

67 s of neonatal Fc receptor (FcRn) binding and complement-dependent cytotoxicity (CDC) activity.

68 induced mouse antibodies mediated effective complement-dependent cytotoxicity (CDC) against the pros

69 ansplant recipients who have positive B-cell complement-dependent cytotoxicity (CDC) along with posit

70 equire NMO-IgG effector function to initiate complement-dependent cytotoxicity (CDC) and antibody-dep

71 85(her2/neu) kinase (ERBB2) but also trigger complement-dependent cytotoxicity (CDC) and antibody-dep

72 plement cascade induces tumor cell lysis via complement-dependent cytotoxicity (CDC) and attracts and

73 orin-4 (AQP4) on astrocytes, which initiates complement-dependent cytotoxicity (CDC) and inflammation

74 -IgG) to astrocyte aquaporin-4 (AQP4) causes complement-dependent cytotoxicity (CDC) and inflammation

75 Both the complement-dependent cytotoxicity (CDC) assay (class I)

76 Using flow cytometry and complement-dependent cytotoxicity (CDC) assays, we have

77 A third strategy used complement-dependent cytotoxicity (CDC) by treating the

78 using bead-based assay as an add-on test to complement-dependent cytotoxicity (CDC) crossmatch with

79 Complement-dependent cytotoxicity (CDC) has been suggest

80 we tested whether EMT confers resistance to complement-dependent cytotoxicity (CDC) in lung cancer c

81 effective than rituximab (RTX) in promoting complement-dependent cytotoxicity (CDC) of B cells via t

82 mab and ofatumumab (OFA), efficiently induce complement-dependent cytotoxicity (CDC) of CD20(+) B cel

83 y-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC) of HIV-1-infecte

84 oward neoplastic cells that can kill without complement-dependent cytotoxicity (CDC) or antibody-depe

85 tibodies has been performed using cell-based complement-dependent cytotoxicity (CDC) techniques.

86 ixing and clinically relevant based upon the complement-dependent cytotoxicity (CDC) test.

87 m was used to measure IgM/IgG binding to and complement-dependent cytotoxicity (CDC) to cells from WT

88 n to regulate numerous biologic processes on complement-dependent cytotoxicity (CDC) was investigated

89 h innate and adaptive immunity, is executing complement-dependent cytotoxicity (CDC) with its C5b-9 p

90 correlated with the extent of cell lysis by complement-dependent cytotoxicity (CDC), and a peptide c

91 ect antiproliferative and apoptotic effects, complement-dependent cytotoxicity (CDC), and antibody-de

92 dependent cell-mediated cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and apoptosis h

93 T- and B-cell complement-dependent cytotoxicity (CDC), flow cytometric

94 ns that stimulated IgG hexamer formation and complement-dependent cytotoxicity (CDC).

95 ficiently by C1q, deposit C3b, and result in complement-dependent cytotoxicity (CDC).

96 tes using the innate immune system including complement-dependent cytotoxicity (CDC).

97 ein 70, plays a role in cell protection from complement-dependent cytotoxicity (CDC).

98 mechanisms that support their resistance to complement-dependent cytotoxicity (CDC).

99 b-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC).

100 ncer therapy depends in part on induction of complement-dependent cytotoxicity (CDC).

101 by monoclonal antibodies, which act through complement-dependent cytotoxicity (CDC).

102 contribute to Ab efficacy against cancer is complement-dependent cytotoxicity (CDC).

103 Disadvantages inherent to complement-dependent cytotoxicity cross-match (CDC XM) m

104 r for the highest risk group with a positive complement-dependent cytotoxicity crossmatch (CDC XM) be

105 splants from deceased donors with a negative complement-dependent cytotoxicity crossmatch (XM) was pe

106 (DSZ) strategies in patients with a negative complement-dependent cytotoxicity crossmatch.

107 The antigens identified to produce positive complement-dependent cytotoxicity crossmatches (XMs; >20

108 ell flow cytometry (FXM) versus conventional complement-dependent cytotoxicity (CXM) in consecutive p

109 homa cell lines tested, as well as increased complement-dependent cytotoxicity in 1 of 3 cell lines,

110 There was evidence of complement-dependent cytotoxicity in several patients.

111 ody-dependent cell-mediated cytotoxicity and complement-dependent-cytotoxicity in GPC3-positive cance

112 ody-dependent cell-mediated cytotoxicity and complement-dependent cytotoxicity, is desirable for ther

113 Patients with a complement-dependent cytotoxicity negative and flow cyto

114 ected patients who underwent ABO-compatible, complement-dependent cytotoxicity-negative crossmatch ki

115 fluorescence intensity [MFI] > 3000) with a complement-dependent cytotoxicity-negative crossmatch, w

116 ed to rituximab-mediated growth reduction or complement-dependent cytotoxicity nor underwent apoptosi

117 The resulting IgG2a response mediated complement-dependent cytotoxicity of a LeY-expressing hu

118 l-dependent cytotoxicity but did not mediate complement-dependent cytotoxicity of HMW-MAA(+) melanoma

119 wn by binding of ch 14.18 to tumor cells and complement-dependent cytotoxicity of posttreatment sera

120 at human MAbs against B5 can potently direct complement-dependent cytotoxicity of vaccinia virus-infe

121 the ability of col(V) immune serum to induce complement-dependent cytotoxicity only in the epithelial

122 When analyzed by complement-dependent cytotoxicity, only 2 of 15 BOS+ pat

123 ivity kill GcSTn-expressing human tumors via complement-dependent cytotoxicity or antibody-dependent

124 cell donor cross-matches using antiglobulin complement-dependent cytotoxicity or flow cytometry woul

125 cytes, or polymorphonuclear cells as well as complement-dependent cytotoxicity positively correlated

126 ls, polymorphonuclear cell-mediated ADCC and complement-dependent cytotoxicity required higher EGFR e

127 n was performed using an anti-human globulin-complement-dependent cytotoxicity technique.

128 nti-A2 and anti-B8,defined in a conventional complement-dependent cytotoxicity test (CDC).

129 recipients of failed cadaveric allografts by complement-dependent cytotoxicity tests and by an enzyme

130 nisms include antibody-, effector cell-, and complement-dependent cytotoxicity, the disruption of CD2

131 ong binding and mediated similarly effective complement-dependent cytotoxicity to GM2-expressing canc

132 Ofatumumab has enhanced capacity for complement-dependent cytotoxicity, whereas obinutuzumab,

133 Furthermore, antibody-mediated complement-dependent cytotoxicity with the antibodies se

134 y to predict T lymphocyte flow cytometry and complement dependent cytotoxicity XM results with the me