ライフサイエンスコーパス: ADCC

1 ADCC and ADP assays were performed using serum samples o

2 ADCC assays confirmed the cytotoxic effects of ARGX-111

3 ADCC is mediated largely by natural killer (NK) cells, w

4 ADCC levels were higher in uninfected than infected infa

5 ADCC was determined by using a fluorometric ADCC assay,

6 ADCC was documented in 80% of PHI enrollment samples and

7 ADCC-Ab titers increased following experimental influenz

8 ADCC-Abs titers directed against H7N9 HA or NA proteins.

9 ADCC-mediating Abs can target more conserved regions of

10 ritical role for NKG2D ligands in anti-HIV-1 ADCC responses.

11 uenza vaccines to induce ADCC-mediating Abs (ADCC-Abs) in adults and children is unclear.

12 However, NAE inhibition affected ADCC minimally.

13 against all 3 TIV hemagglutinins, and in all ADCC assays tested.

14 Although ADCC has been suggested to protect against HIV, the rela

15 agent, we engineered the same antibody in an ADCC-inactive form that is similarly capable of blocking

16 aR) by Abs, which is required to initiate an ADCC response.

17 These data demonstrate that ADCP and ADCC are impaired by antigenic modulation and that ADCP

18 -specific Fc receptor-binding antibodies and ADCC against HIV-1-infected cells in vitro These results

19 engineered for increased FcgRIII binding and ADCC capacity.

20 ed gp140 antigen induced superior B-cell and ADCC responses, and the elevated B-cell responses proved

21 says, we compared ADCC-mediating antibodies (ADCC-Abs) in sera collected from healthy infants, childr

22 V-1 developed additional mechanisms to avoid ADCC, including Vpu-mediated BST-2 antagonism, which dec

23 vitro FcgammaR-binding analyses, cell-based ADCC assays, and in vivo IgG-mediated cellular depletion

24 ADCC antibodies prevaccination, but baseline ADCC was not predictive of HAI vaccine responsiveness.

25 demonstrating a positive association between ADCC and slower disease progression, it is possible that

26 Significant associations between ADCC and disease progression were found only after remov

27 We found no correlation between ADCC responses to the H7 HA and either influenza virus-s

28 s failed to demonstrate correlations between ADCC and disease progression, and they also contribute t

29 ovide insights into the relationship between ADCC and neutralization important for the development of

30 A(H1N1)pdm09 exposure did not boost ADCC responses specific for H7 HA antigens.

31 However, rituximab's ability to elicit both ADCC and ADCP was reduced by antigenic modulation, where

32 iated elimination of HIV-1-infected cells by ADCC and utilized it to demonstrate that LSEVh-LS-F rapi

33 le that continued stimulation of NK cells by ADCC during chronic HIV infection could render these cel

34 anced their susceptibility to elimination by ADCC.

35 their surface are preferentially targeted by ADCC mediated by HIV-positive (HIV(+)) sera.

36 in the exposure of Env epitopes targeted by ADCC-mediating antibodies at the surface of cells expres

37 f HIV-1 Env that is specifically targeted by ADCC-mediating antibodies present in sera from HIV-1-inf

38 avian H7N9 subtype of influenza A virus, by ADCC and CDL assays.

39 Autosomal dominant congenital cataracts (ADCC) are clinically and genetically heterogeneous disea

40 tion and NK cytotoxicity assays, we compared ADCC-mediating antibodies (ADCC-Abs) in sera collected f

41 ion in antibody-dependent cell cytotoxicity (ADCC).

42 nd antibody-dependent cellular cytotoxicity (ADCC) activity after immunization with the DNA prime-pro

43 nt antibody-dependent cellular cytotoxicity (ADCC) activity in the Thai RV144 vaccine trial was sugge

44 ed antibody-dependent cellular cytotoxicity (ADCC) activity strongly inhibited the severity of murine

45 th antibody-dependent cellular cytotoxicity (ADCC) activity.

46 gh antibody-dependent cellular cytotoxicity (ADCC) activity.

47 ct antibody-dependent cellular cytotoxicity (ADCC) against actively infected cells, and ultimately th

48 te antibody-dependent cellular cytotoxicity (ADCC) against avian influenza virus subtypes, including

49 ed antibody-dependent cellular cytotoxicity (ADCC) against the Env V2 and constant 1 (C1) regions.

50 ed antibody-dependent cellular cytotoxicity (ADCC) against tumor cells.

51 ly antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent phagocytosis (ADP), are unc

52 ed antibody-dependent cellular cytotoxicity (ADCC) and their presence correlated with poor clinical o

53 te antibody-dependent cellular cytotoxicity (ADCC) by aggregating FcgammaRIIIA/CD16, contributing sig

54 ve antibody-dependent cellular cytotoxicity (ADCC) by allowing more effective binding of the Fc regio

55 ng antibody-dependent cellular cytotoxicity (ADCC) effector functions.

56 by antibody-dependent cellular cytotoxicity (ADCC) effector responses.

57 th antibody-dependent cellular cytotoxicity (ADCC) function at the peak immunity time point, which wa

58 te antibody-dependent cellular cytotoxicity (ADCC) have been shown to be present in sera from most HI

59 ic antibody-dependent cellular cytotoxicity (ADCC) in controlling viral infection and replication.

60 Antibody-dependent cellular cytotoxicity (ADCC) is mediated through the engagement of the Fc segme

61 mediate Ab-dependent cellular cytotoxicity (ADCC) largely contributes to the clinical success of ant

62 Antibody-dependent cellular cytotoxicity (ADCC) may be an important component of protection agains

63 e, antibody-dependent cellular cytotoxicity (ADCC) may play a role in cross-protective immunity to in

64 in antibody-dependent cellular cytotoxicity (ADCC) may provide some protection from influenza virus i

65 by antibody-dependent cellular cytotoxicity (ADCC) requires the presence of envelope glycoproteins (E

66 Ab-dependent cellular cytotoxicity (ADCC) responses are of growing interest in the HIV vacci

67 nd antibody-dependent cellular cytotoxicity (ADCC) responses.

68 ve antibody-dependent cellular cytotoxicity (ADCC) responses.

69 ng antibody-dependent cellular cytotoxicity (ADCC) to eliminate infected cells following reactivation

70 of antibody-dependent cellular cytotoxicity (ADCC) to eliminate reactivated latent HIV-1-infected cel

71 ze antibody-dependent cellular cytotoxicity (ADCC) to eliminate the HIV-1-infected cells and thereby

72 ntial of Ab-dependent cellular cytotoxicity (ADCC) to slow disease progression following HIV infectio

73 NK cell Ab-dependent cellular cytotoxicity (ADCC) triggered via FcgammaR-IIIA (CD16) in the response

74 ic antibody-dependent cellular cytotoxicity (ADCC) will help in understanding its role in HIV immunit

75 ncluding Ab-dependent cellular cytotoxicity (ADCC), Ab-dependent cell-mediated viral inhibition, and

76 oxicity, Ab-dependent cellular cytotoxicity (ADCC), Ab-dependent cellular phagocytosis (ADCP), and in

77 s, antibody-dependent cellular cytotoxicity (ADCC), and low-titer tier 1B and tier 2 neutralizing ant

78 ed antibody-dependent cellular cytotoxicity (ADCC), and mice that received the MAbs and were then cha

79 al antibody-dependent cellular cytotoxicity (ADCC), and modest antibody-dependent cell-mediated virus

80 n, antibody-dependent cellular cytotoxicity (ADCC), infected cell binding, and inhibition of viral at

81 te antibody-dependent cellular cytotoxicity (ADCC), the killing of an antibody-coated virus-infected

82 to antibody-dependent cellular cytotoxicity (ADCC), we treated cells with the Nedd8 activation enzyme

83 es antibody-dependent cellular cytotoxicity (ADCC), whereas terminal alpha2,6-sialylation plays a cri

84 is antibody-dependent cellular cytotoxicity (ADCC), whereby host antibodies bind envelope glycoprotei

85 ic antibody-dependent cellular cytotoxicity (ADCC)-activating antibodies are readily detected in heal

86 ia antibody-dependent cellular cytotoxicity (ADCC)-like mechanism, increase IFNgamma production after

87 ic antibody-dependent cellular cytotoxicity (ADCC)-mediating antibodies.

88 ed antibody-dependent cellular cytotoxicity (ADCC).

89 ed antibody-dependent cellular cytotoxicity (ADCC).

90 te antibody-dependent cellular cytotoxicity (ADCC).

91 gh antibody-dependent cellular cytotoxicity (ADCC).

92 gets via Ab-dependent cellular cytotoxicity (ADCC).

93 by antibody-dependent cellular cytotoxicity (ADCC).

94 mediated Ab-dependent cellular cytotoxicity (ADCC).

95 te antibody-dependent cellular cytotoxicity (ADCC).

96 ed antibody-dependent cellular cytotoxicity (ADCC).

97 te antibody-dependent cellular cytotoxicity (ADCC).

98 to antibody-dependent cellular cytotoxicity (ADCC).

99 tibody-dependent cell-mediated cytotoxicity (ADCC) and complement-mediated cytotoxicity in vitro, and

100 tibody-dependent cell-mediated cytotoxicity (ADCC) and virus neutralization that may help to guide th

101 tibody-dependent cell-mediated cytotoxicity (ADCC) assay, and immunohistochemistry.

102 tibody-dependent cell-mediated cytotoxicity (ADCC) assays indicate that this protection is antibody m

103 tibody-dependent cell-mediated cytotoxicity (ADCC) assays revealed that the cell surface DPP4 prefere

104 tibody-dependent cell-mediated cytotoxicity (ADCC) by non-neutralizing antibodies (nnAbs) specific to

105 tibody-dependent cell-mediated cytotoxicity (ADCC) by selective desialylation of the tumor cell glyco

106 tibody-dependent cell-mediated cytotoxicity (ADCC) has been little studied.

107 targets via FcgammaR-mediated cytotoxicity (ADCC), a short-term process.

108 tibody-dependent cell-mediated cytotoxicity (ADCC), and conversely that RNAi knockdown of tetherin, b

109 tibody-dependent cell-mediated cytotoxicity (ADCC), in prevention of human immunodeficiency virus typ

110 tibody-dependent cell-mediated cytotoxicity (ADCC), we show that substitutions in this motif increase

111 tibody-dependent cell-mediated cytotoxicity (ADCC).

112 dy-dependent cellular-mediated cytotoxicity (ADCC).

113 tibody-dependent cell-mediated cytotoxicity (ADCC).

114 tibody-dependent cell-mediated cytotoxicity (ADCC).

115 tibody-dependent cell-mediated cytotoxicity (ADCC).

116 tibody-dependent cell-mediated cytotoxicity (ADCC).

117 ert Ab-dependent cell-mediated cytotoxicity (ADCC).

118 tibody-dependent cell-mediated cytotoxicity (ADCC).

119 s (antibody-dependent cellular cytotoxicity [ADCC]) or complement (complement-dependent lysis [CDL]).

120 (termed "Ab-dependent cellular cytotoxicity [ADCC]-mediating Abs"), may assist in protective immunity

121 d BST-2 downregulation was shown to decrease ADCC responses by limiting the amount of Env present at

122 of core fucosylation significantly decreased ADCC in a cell-based assay and suppressed antibody-media

123 Furthermore, although we detect ADCC activities of F240 against cells spinoculated with

124 er, and high responder groups had detectable ADCC antibodies prevaccination, but baseline ADCC was no

125 s for Env epitopes that constitute effective ADCC targets is of fundamental interest for humoral anti

126 ha, respectively) are required for efficient ADCC activity and that antibodies specific for the recep

127 inea pigs and found that the sgp140 elicited ADCC-mediating antibodies.

128 seful in vaccine regimens aimed at eliciting ADCC responses.

129 antibodies and support a role for eliciting ADCC-mediating IgG1 in HIV vaccines.

130 ted BST-2 downregulation and greatly enhance ADCC responses against HIV-1-infected cells in the prese

131 t modification of the Fc fragment to enhance ADCC can be an effective strategy to augment the efficac

132 more, CD16A-158V and G1m3 allotypes enhanced ADCC against opsonized HSV-1-infected fibroblasts.

133 trials has been associated with the enhanced ADCC provided by these engineered mAbs.

134 ialidase conjugation to trastuzumab enhanced ADCC against tumor cells expressing moderate levels of H

135 Yet, enhanced ADCC was observed among NK cells showing a differentiate

136 ated mechanisms to avoid the exposure of Env ADCC epitopes by downregulating CD4 and by limiting the

137 cells infected with HIV-1JR-FL or SHIVAD8-EO ADCC activity generally correlated with antibody binding

138 Older adults commonly have pre-existing ADCC antibodies in the absence of high HAI titers to cir

139 or-restricted expression of NKG2DL, NKG2D-Fc-ADCC may constitute an attractive means for immunotherap

140 ADCC was determined by using a fluorometric ADCC assay, before and after removal of plasma IgA.

141 V5 do not represent a major determinant for ADCC responses mediated by sera from HIV-1-infected indi

142 9 of the gp120 inner domain is important for ADCC mediated by anti-cluster A antibodies and sera from

143 ed patients and possibly reduce the risk for ADCC-mediated ABMR.

144 the data best, but with a role suggested for ADCC or other infected cell clearance mechanisms.

145 mary HIV-1-infected cells can be targets for ADCC mediated by autologous serum antibodies and innate

146 m HIV-1(+) subjects were used as targets for ADCC.

147 lizing antibodies, were therefore tested for ADCC against cells infected with a lab-adapted HIV-1 iso

148 al that Vpu protects HIV-infected cells from ADCC as a function of its ability to counteract tetherin

149 ated strategies to conceal Env epitopes from ADCC-mediating antibodies present in HIV+ sera.

150 sists despite this drug to allow escape from ADCC.

151 nding and induce similar effector functions (ADCC and ADCP) in the absence of nonspecific, endogenous

152 H7 HA ADCC responses were variable longitudinally within donor

153 All donors had ADCC responses against 2009 pandemic influenza A(H1N1) v

154 lly, we assessed the ability of low and high ADCC-Ab titers to protect adults from experimental chall

155 d 28 post-DAC) revealed significantly higher ADCC in samples at day 28 post-DAC when compared with pr

156 Together, our results show how ADCC provides a therapeutic advantage over conventional

157 lation, sialylation did not adversely impact ADCC.

158 Importantly, ADCC mediated against these primary cells could be enhan

159 tumor cell lines, whereas no differences in ADCC by MNC or PMN were detected.

160 Increase in ADCC antibody activity in infected infants was associate

161 eived a dose of ISV had a robust increase in ADCC-Ab titers to both recombinant hemagglutinin (rHA) p

162 s not sufficient to stimulate an increase in ADCC-competent antibodies, despite viral rebound in all

163 mouse IgG2a, hIgG1 mAbs were ineffective in ADCC assays with murine natural killer cells as effector

164 e I and II antibodies of various isotypes in ADCC and antibody-dependent cellular-phagocytosis (ADCP)

165 ressing, nonclassical monocytes resulting in ADCC-mediated lysis of regulatory T cells (Tregs).

166 or-mediated functional activities, including ADCC and antibody-dependent cellular phagocytosis (ADCP)

167 cific effector antibody responses, including ADCC and ADP.

168 Indeed, ADCC-Abs to NPs of seasonal H1N1 and H3N2 viruses correl

169 The ability of influenza vaccines to induce ADCC-mediating Abs (ADCC-Abs) in adults and children is

170 Infant ADCC positively correlated with the magnitude of IgG1 bi

171 analyzed how KIR/HLA interactions influence ADCC induced by rituximab and by GA101, a novel type II

172 tor was demonstrated to positively influence ADCC responses.

173 Interestingly, ADCC and HAI responses tracked closely across all groups

174 vaccinated humans showed not only high-level ADCC and ADCP activities but also cross-subtype ADCC and

175 We also measured ADCC-Abs in children who either received a dose of triva

176 ich correlated with their ability to mediate ADCC responses against HIV-1-infected cells, exposing th

177 gage hFcgammaRIIIA on macrophages to mediate ADCC, but also engage hFcgammaRIIA, the sole hFcgammaR e

178 head domain of HA therefore fail to mediate ADCC.

179 In vitro analysis of 3F8-mediated ADCC showed that KIR3DL1(-) and 3DS1(+) NK cells were in

180 Evaluation of BI 836858-mediated ADCC in serial marrow AML aspirates in patients who rece

181 blocked using antibodies, BI 836858-mediated ADCC was significantly decreased, suggesting that DAC en

182 t only HA stalk-specific antibodies mediated ADCC efficiently and displayed cross-reactivity with IBV

183 rovement in NK92MI-transfected CD16-mediated ADCC, a 6-fold improvement in CD32-mediated ADCC, and a

184 ADCC, a 6-fold improvement in CD32-mediated ADCC, and a 2.5-fold improvement in complement-mediated

185 peak ADCC antibody titres, NK cell-mediated ADCC and antibody-mediated activation of MIP-1beta in NK

186 ompromise BI 836858-induced NK-cell-mediated ADCC.

187 e of modifying the magnitude of IgG-mediated ADCC in HIV infection, mitigating its beneficial effect.

188 cell receptor-specific manner, (ii) mediated ADCC, and (iii) reduced ocular disease in virus-infected

189 Furthermore, monocyte-mediated ADCC against cetuximab-coated tumor targets was enhanced

190 ed cytolytic functions of NK cells mediating ADCC.

191 Although MNC-ADCC was not affected by C5 cleavage, the cytotoxic acti

192 To more effectively mobilize ADCC, we designed and constructed LSEVh-LS-F, a broadly

193 In orthotopic mammary carcinoma models, ADCC enhancement was crucial to deplete circulating tumo

194 gp120-specific IgA was capable of modifying ADCC responses during natural HIV infection for the firs

195 reatment with anti-GD2 mAb that relies on NK-ADCC.

196 ween viral recrudescence and the boosting of ADCC antibodies, which has implications for strategies t

197 ligand was absent were the main effectors of ADCC in these donors.

198 8 agonist treatment, and this enhancement of ADCC required granzyme B.

199 f HIV-1 Vpu, which contributes to evasion of ADCC, could potentially sensitize infected cells to this

200 sophisticated mechanism to avoid exposure of ADCC-mediating Env epitopes by down-regulating CD4 and b

201 activities and were distinct from a group of ADCC assays that showed a more similar response profile

202 Although the induction of ADCC-mediating antibodies in HIV-infected subjects has b

203 t always predictive of ADCC, as instances of ADCC in the absence of detectable neutralization, and vi

204 thus our results suggest the involvement of ADCC and associated inflammation in pathogenesis of LBP.

205 ne whether IgA could modify the magnitude of ADCC in HIV infection, abrogating its protective role.

206 from 12-month PHI samples: the magnitude of ADCC not only increased after IgA removal but also corre

207 nti-V regions 1 and 2 Abs may be a marker of ADCC breadth.

208 correlated well with a functional measure of ADCC as well as IgG subclasses.

209 Mobilization of ADCC may facilitate elimination of reactivated latent HI

210 further investigation into the potential of ADCC to eliminate reactivated latently infected cells is

211 neutralization was not always predictive of ADCC, as instances of ADCC in the absence of detectable

212 V vaccine should stimulate the production of ADCC-mediating IgG antibodies but not IgA.

213 ctivation may contribute to the reduction of ADCC in sensitized patients and possibly reduce the risk

214 l for the further analysis and refinement of ADCC-inducing HIV and other antiviral vaccine regimens.

215 plays an important role in the regulation of ADCC, and that cross-talk among antibodies of varying sp

216 us, but we unexpectedly found high titers of ADCC antibodies to the H7N9 subtype virus in all sera fr

217 High titers of ADCC-Abs against H7N9 virus-infected cells were detected

218 here was no detectable increase in titers of ADCC-Abs to rHA or virus-infected cells in adults and ch

219 offer a preclinical rationale for the use of ADCC-optimized antibodies to treat tumors harboring this

220 tigate the influence of the Phe 43 cavity on ADCC responses.

221 ific combinations of sugars in the glycan on ADCC remains to be further addressed, however.

222 In contrast, the effect of sialylation on ADCC was dependent on the status of core fucosylation.

223 nificantly influence HSV-1 susceptibility or ADCC.

224 antibody binding to HIV-infected cells, peak ADCC antibody titres, NK cell-mediated ADCC and antibody

225 enhanced complement receptor 3-dependent PMN-ADCC against tumor cells.

226 Potentially, ADCC-mediating antibodies directed to the HA stalk of IB

227 Higher titers (>/=320) of preexisting ADCC-Abs were associated with lower virus replication an

228 h resulted in a modest degree of protection, ADCC responses were identified as being part of the corr

229 We quantified ADCC-Abs in serum samples from adults who received a dos

230 preparations contain broadly cross-reactive ADCC mediating antibodies.

231 ated blockade of NKG2D significantly reduced ADCC of cells infected with viruses carrying Nef from EC

232 ylation of IgG is a "safety switch" reducing ADCC, thus our results suggest the involvement of ADCC a

233 infected PBMCs in a physiologically relevant ADCC model, highlighting the interest in inducing such A

234 d antibody-dependent cytotoxicity responses (ADCC) after DC-targeting boosts.

235 Serum ADCC activity was analyzed using Fc receptor cross-linki

236 A potential barrier is that HIV-1-specific ADCC antibodies decline in patients on long-term antiret

237 es and effectively mobilizing HIV-1-specific ADCC to eliminate HIV-1-infected cells.

238 t antigenic stimulus to boost HIV-1-specific ADCC.

239 uction in HIV type 1 envelope (Env)-specific ADCC-mediated killing of target cells (P<.001) was obser

240 ant reduction in the ability of Env-specific ADCC antibodies to activate natural killer cells (P<.001

241 apeutic benefit of pre-existing HIV-specific ADCC antibodies and support a role for eliciting ADCC-me

242 t HIV, the relationship between HIV-specific ADCC antibodies at the time of HIV exposure and infectio

243 C and ADCP activities but also cross-subtype ADCC and ADCP activities when a polyvalent DNA prime-pro

244 l (P < 0.001) response kinetics and superior ADCC (P < 0.014) in a group receiving the CD4bs-occluded

245 Targeting ADCC-Abs to internal proteins may be a potential mechani

246 Further analysis showed that ADCC-Abs titers were significantly higher toward H7N9 NP

247 Our results suggest that ADCC might be an active immune mechanism in EC that help

248 Our results suggest that ADCC plays a role in cross-protective immunity against i

249 possibly chronic rejection, and suggest that ADCC-mediated injury may increase in strategies aimed at

250 ts further identified distinctions among the ADCC assays.

251 We evaluated the ADCC activity of passively acquired antibodies in infant

252 wer fucosylation levels and thus improve the ADCC of these proteins.

253 ermore, it underscores the complexity of the ADCC phenomenon and will help in an understanding of its

254 An improved understanding of the ADCC response to influenza vaccination in older adults i

255 V-1 CRF01_AE decreased the efficiency of the ADCC response.

256 d the impact of EC and progressor Nef on the ADCC susceptibility of HIV-1-infected cells.

257 Prompted by these results, we optimized the ADCC-enhanced molecule for clinical development, generat

258 s and primary virus isolates, we studied the ADCC profile of different monoclonal Abs targeting the V

259 anced antibody was more efficacious than the ADCC-inactive antibody.

260 ent tumor xenografts, we determined that the ADCC-enhanced antibody was more efficacious than the ADC

261 We compared their ADCC activity to some bNAbs targeting different regions

262 little is known about the kinetics of these ADCC responses.

263 Thus, ADCC-defective Fn14-blocking antibodies are not only pos

264 he susceptibility of HIV-1-infected cells to ADCC as a result of tetherin-mediated retention of buddi

265 f CD4mc to sensitize HIV-1-infected cells to ADCC by sera from HIV-1-infected individuals.IMPORTANCE

266 he susceptibility of HIV-1-infected cells to ADCC despite the activity of Vpu.

267 tibility of HIV-1- and SIV-infected cells to ADCC in a manner that directly correlates with elevated

268 ted ex vivo-amplified primary CD4 T cells to ADCC killing mediated by autologous sera and effector ce

269 ed susceptibility of HIV-1-infected cells to ADCC may contribute to the EC phenotype.

270 mation and sensitize HIV-1-infected cells to ADCC mediated by HIV+ sera.

271 he susceptibility of HIV-1-infected cells to ADCC mediated by HIV-positive (HIV+) sera.

272 cing the susceptibility of infected cells to ADCC mediated by this class of antibodies.

273 susceptibility of EC HIV-1-infected cells to ADCC responses.IMPORTANCE Attenuated Nef functions have

274 ed susceptibility of HIV-1-infected cells to ADCC.

275 these two genes sensitized infected cells to ADCC.

276 ncreased susceptibility of infected cells to ADCC.

277 ith Env and thereby sensitize these cells to ADCC.

278 y be required to sensitize infected cells to ADCC.

279 the susceptibility of HIV-infected cells to ADCC.

280 he susceptibility of HIV-1-infected cells to ADCC.

281 ects the susceptibility of infected cells to ADCC.

282 ells infected with primary HIV-1 isolates to ADCC mediated by antibodies present in sera, cervicovagi

283 ed cells were considerably more sensitive to ADCC, both in terms of the number of antibodies and magn

284 s correlated with enhanced susceptibility to ADCC.

285 mation, thereby increasing susceptibility to ADCC.

286 d render HIV-1-infected cells susceptible to ADCC and thus have therapeutic utility.

287 d primary cells were modestly susceptible to ADCC mediated by autologous or heterologous HIV-1(+) ser

288 ent and leaves infected cells susceptible to ADCC.

289 ay act as the molecular mechanism underlying ADCC, which further confirms the role of Cx50 in the mai

290 to generate anti-tumor T cell responses upon ADCC-mediated tumor clearance.

291 In older vaccinees, ADCC response mirrored HAI antibodies and was readily de

292 h-LS-F to eliminate HIV-1-infected cells via ADCC combined with its broad neutralization activity sup

293 h-LS-F to eliminate HIV-1-infected cells via ADCC combined with its broad neutralization activity sup

294 ty by surface plasmon resonance and in vitro ADCC potency with a cell based bioassay.

295 lectively inhibit rituximab-induced in vitro ADCC toward target cells expressing cognate HLA KIR liga

296 eated with anti-HLA antibody+ sera (in vitro ADCC), with or without immunosuppressive agents.

297 rse effect on FcgammaRIIIA binding, in vitro ADCC, and in vivo IgG-mediated cellular depletion, regar

298 to stimulate cross-reactive antibodies with ADCC function may provide an important measure of protec

299 A and Cx50R76H mutations are associated with ADCC and expands the mutation spectrum of Cx50 in associ

300 or NA proteins, and correlated strongly with ADCC-Abs titers against H7N9 virus-infected cells.

301 N1 and H3N2 viruses correlated strongly with ADCC-Abs to H7N9 NP, suggesting that seasonal influenza