ライフサイエンスコーパス: ADCC

1 ADCC activity significantly higher than seronegative con

2 ADCC activity was also found to be independent of HIV st

3 ADCC against HIV-infected target cells was elicited in r

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

5 ADCC was determined by using a fluorometric ADCC assay,

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

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

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

9 d by the extended NA and includes additional ADCC-active antibodies.

10 D Ig although fucosylation varied, affecting ADCC activity.

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

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

13 Imlifidase inhibited NK cell activation and ADCC in vitro and in treated patients.

14 IdeS inhibited NK cell activation and ADCC in vitro and in treated patients.

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

16 ding, as well as neutralizing antibodies and ADCC responses.

17 t a broad panel of Env and Gag antigens, and ADCC responses were observed in the groups throughout th

18 tance; it can increase rituximab binding and ADCC activity in vitro and can synergistically improve a

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

20 y-mediated NK cell activation (Allo-CFC) and ADCC in vitro.

21 y-mediated NK cell activation (Allo-CFC) and ADCC in vitro.

22 shion to promote FcgammaRIIIa engagement and ADCC.IMPORTANCE The "open" CD4-bound conformation of HIV

23 ed interchain disulfide bonds reoxidize, and ADCC activity is restored.

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

25 ovo Env expression, resulting in artifactual ADCC measurements.

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

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

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

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

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

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

32 d Chinese hamster ovary (CHO) mAb-Ds blocked ADCC and clearance.

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

34 ADE conditions, NK cells can be activated by ADCC Abs and can control the magnitude of ADE.

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

36 anced their susceptibility to elimination by ADCC.

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

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

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

40 gesting the coexistence of the counteractive ADCC Abs, in the same ADE-serum, capable of strongly pro

41 y 2C6 having Ab-dependent cell cytotoxicity (ADCC) against envelope proteins from two clades.

42 investigates Ab-dependent cell cytotoxicity (ADCC) in counteracting ADE.

43 Ab-dependent cell cytotoxicity (ADCC) is a common effector function for nonneutralizing

44 specific Ab-dependent cellular cytotoxicity (ADCC) activity at levels comparable with NK cells on a p

45 ng antibody-dependent cellular cytotoxicity (ADCC) activity in a reporter assay.

46 nd antibody-dependent cellular cytotoxicity (ADCC) activity of the mAbs tested.

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

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

49 le antibody-dependent cellular cytotoxicity (ADCC) activity.

50 nd antibody-dependent cellular cytotoxicity (ADCC) activity.

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

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

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

54 as antibody-dependent cellular cytotoxicity (ADCC) and phagocytosis, are mediated by FcgammaRs, which

55 ic antibody-dependent cellular cytotoxicity (ADCC) antibodies within HIV-1-positive (HIV-1(+)) indivi

56 er antibody-dependent cellular cytotoxicity (ADCC) antibody activity, whereas animals immunized by th

57 ve antibody-dependent cellular cytotoxicity (ADCC) as IgG1 ab1 had ADCC activity in vitro.

58 An antibody-dependent cellular cytotoxicity (ADCC) assay was used to determine whether an S8mAb can d

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

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

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

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

63 ve antibody-dependent cellular cytotoxicity (ADCC) in HIV-1 and HIV-2 monoinfection or dual infection

64 ent antibody-mediated cellular cytotoxicity (ADCC) in vaccine-induced protection.

65 ve antibody-dependent cellular cytotoxicity (ADCC) in vitro resulted in arming of effector cells in v

66 Antibody-dependent cellular cytotoxicity (ADCC) is a key effector mechanism of natural killer (NK)

67 Ab-dependent cellular cytotoxicity (ADCC) is one of the most important effector mechanisms o

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

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

70 he antibody-dependent cellular cytotoxicity (ADCC) mechanism, as anti-CTLA4 without the FcgammaR-bind

71 ce antibody-dependent cellular cytotoxicity (ADCC) of alphavbeta3-expressing tumor cells despite thei

72 a strong Ab-dependent cellular cytotoxicity (ADCC) response for all animals, as opposed to the Ab-dep

73 nd antibody-dependent cellular cytotoxicity (ADCC) responses against gp120-coated target cells were s

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

75 ic antibody-dependent cellular cytotoxicity (ADCC) responses with protection from and delayed progres

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

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

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

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

80 Antibody-dependent cellular cytotoxicity (ADCC) was measured by a bioluminescence reporter assay.

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

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

83 er antibody-dependent cellular cytotoxicity (ADCC), and better neutralizing and stronger cross-protec

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

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

86 nt antibody-dependent cellular cytotoxicity (ADCC), making them an important vaccine target.

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

88 om antibody-dependent cellular cytotoxicity (ADCC), which is often mediated by antibodies that requir

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

90 of antibody-dependent cellular cytotoxicity (ADCC)-mediating antibodies present in HIV-positive (HIV(

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

92 tibody (Ab)-dependent cellular cytotoxicity (ADCC)-mediating antibodies.

93 nd antibody-dependent cellular cytotoxicity (ADCC).

94 to antibody-dependent cellular cytotoxicity (ADCC).

95 to antibody-dependent cellular cytotoxicity (ADCC).

96 of antibody-dependent cellular cytotoxicity (ADCC).

97 ed antibody-dependent cellular cytotoxicity (ADCC).

98 te antibody-dependent cellular cytotoxicity (ADCC).

99 to antibody-dependent cellular cytotoxicity (ADCC).

100 ed antibody-dependent cellular cytotoxicity (ADCC).

101 te antibody-dependent cellular cytotoxicity (ADCC).

102 ed antibody-dependent cellular cytotoxicity (ADCC).

103 to antibody-dependent cellular cytotoxicity (ADCC).

104 e host antibody (AB)-dependent cytotoxicity (ADCC) on HCMV is still unclear.

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

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

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

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

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

110 tibody-dependent cell-mediated cytotoxicity (ADCC) is an important mechanism of action for many thera

111 tibody-dependent cell-mediated cytotoxicity (ADCC) is an important pathway responsible for antibody-m

112 tibody-dependent cell-mediated cytotoxicity (ADCC) may play a dominant role in protection.

113 tibody-dependent cell-mediated cytotoxicity (ADCC) responses against EBOV and SUDV.

114 ing Ab-dependent cell-mediated cytotoxicity (ADCC), complement deposition, and complement-dependent c

115 tibody-dependent cell-mediated cytotoxicity (ADCC), during HCV infection is poorly defined, while no

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

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

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

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

120 ro antibody-dependent cellular cytotoxicity [ADCC] activity) than the wild-type PR8 virus, while anti

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

122 cgamma receptor IIIa, resulting in decreased ADCC activity of the IgG(1) antibody.

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

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

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

126 Afucosylation consistently induced efficient ADCC, even at very low Ag density, where fucosylated tar

127 th <50% fucosylation mediated more efficient ADCC and clearance than anti-D Ig.

128 where fucosylated target Abs did not elicit ADCC.

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

130 ient mice pretreated with DARA, and enhanced ADCC activity against CD38-expressing MM cell lines and

131 e functionally mature and exhibited enhanced ADCC against multiple tumor targets.

132 ntribute to skewing NK cells toward enhanced ADCC during infections such as malaria.

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

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

135 We evaluated ADCC mediated by different combinations of 2 to 6 neutra

136 ults have implications for studies examining ADCC against cells with nascent HIV-1 infection.

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

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

139 For ADCC, normal PBMCs were incubated with Farage B (FB) cel

140 For ADCC, normal PBMCs were incubated with Farage B cells (F

141 mbrane as an important inhibitory factor for ADCC.

142 ved models to address the potential role for ADCC against cells with nascent HIV-1 infection.IMPORTAN

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

144 c gamma receptor activation, a surrogate for ADCC function.

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

146 (Allo-CFC-2) in Allo-CFC, and serum used for ADCC were preincubated with IdeS.

147 (Allo-CFC-2) in Allo-CFC, and serum used for ADCC were preincubated with imlifidase.

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

149 cellular cytotoxicity (ADCC) as IgG1 ab1 had ADCC activity in vitro.

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

151 route had higher ADCC antibody activity.

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

153 hs posttransplantation in these, with higher ADCC observed in viremic patients.

154 However, ADCC responses were not associated with KS development o

155 ls and its efficacy was enhanced with L-ICON ADCC in vitro.

156 booster not only induced gp140-specific IgG, ADCC (antibody-dependent cellular cytotoxicity) and some

157 lation, sialylation did not adversely impact ADCC.

158 Importantly, ADCC of early infected cells appeared to be driven by a

159 elf engineered NK cell therapy with improved ADCC properties to treat malignancies that are otherwise

160 In ADCC and other Ab-dependent activation of myeloid effect

161 FB cell% (11 +/- 3% vs. 4 +/- 2%, p=0.02) in ADCC.

162 ll% (11 +/- 3% versus 4 +/- 2%, P = 0.02) in ADCC.

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

164 products whose mechanism of action includes ADCC.

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

166 anticancer monoclonal antibodies to increase ADCC and antitumor efficacy, have been initiated.

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

168 te conformational changes in Env that induce ADCC in the presence of a small-molecule CD4-mimetic com

169 CD4(+) T cells exposes epitopes that induce ADCC.

170 d in glycoprotein-D (DeltagD-2) that induces ADCC provided complete protection against HSV disease an

171 tor was demonstrated to positively influence ADCC responses.

172 ammaRIIIa-Val/Phe158 polymorphism influenced ADCC potency, with NK cells expressing the Val158 varian

173 owledge on the principal factors influencing ADCC potential by therapeutic Abs.

174 ')2 and Fc fragments, potentially inhibiting ADCC.

175 an efficiently activate NK cells, initiating ADCC and killing multiple types of tumor cells, includin

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

177 odies against HIV-2, which mediate intertype ADCC, might contribute to control of HIV-1 during dual i

178 noclonal antibody lost more than half of its ADCC activity after heat stress at 40 degrees C for 4 mo

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

180 1 infection provides a rationale to leverage ADCC-mediating antibodies for treatment purposes.

181 required to engage FcgammaRIIIa and mediate ADCC.

182 tibodies with improved capacities to mediate ADCC.

183 Abs to engage Fc-gamma receptors to mediate ADCC.

184 head domain of HA therefore fail to mediate ADCC.

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

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

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

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

189 We observed NK cell-mediated ADCC of HIV-1-infected cells at multiple stages of CD4 d

190 trate that the magnitude of NK cell-mediated ADCC responses is predominantly influenced by Ag density

191 ive factors affecting human NK cell-mediated ADCC, namely: 1) Ag density, 2) target cell membrane com

192 D4, were all susceptible to NK cell-mediated ADCC.

193 ng DARA therapy could maximize DARA-mediated ADCC against MM cells and deepen the response.

194 iffered in efficacy in FcgammaRIIIa-mediated ADCC assays and clinical trials.

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

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

197 placentally or from breastmilk that mediated ADCC.

198 e conserved gp120 inner domain and mediating ADCC.

199 Antibodies mediating ADCC provide significant protection against neonatal HSV

200 that anti-KSHV Abs are capable of mediating ADCC responses against infected human cells undergoing l

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

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

203 The ability of ADCC to protect the immune-privileged eye, however, may

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

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

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

207 In addition, higher levels of ADCC were observed by FEA and CD107 assay in R+ patients

208 ited a positive correlation with the loss of ADCC activity.

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

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

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

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

213 Mobilization of ADCC may facilitate elimination of reactivated latent HI

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

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

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

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

218 understanding of the epitope specificity of ADCC-mediating Abs is essential for developing effective

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

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

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

222 to confirm the effect of N325 deamidation on ADCC.

223 philic Abs) determine the blocking effect on ADCC.

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

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

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

227 ucture of a vaccine-induced broad and potent ADCC-mediating C1C2-specific MAb showed that it bound a

228 ssing the Val158 variant showing more potent ADCC.

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

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

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

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

233 rmore, the magnitude of HIV-1 cross-reactive ADCC activity during HIV-2 infections depended on the HI

234 mmed death receptor 1 expression and reduced ADCC activity at baseline.

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

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

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

238 DAA treatment restored ADCC ability and reduced programmed death receptor 1 exp

239 Rituximab ADCC induction in Raji2R cells was 20% +/- 2% of that in

240 le in the major clades of HIV and has robust ADCC activity, further definition and appreciation of ta

241 For the clades tested, 2C6 has robust ADCC.

242 mally engage FcgammaRIIIa and mediate robust ADCC.

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

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

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

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

247 iral infection and suggest that HIV-specific ADCC is a function CD8 T cells use to target HIV-infecte

248 t boosting increased clonal lineage-specific ADCC breadth and potency.

249 We show that a strong ADCC is elicited after transplantation and is especially

250 crease in FcgammaR engagement and subsequent ADCC effector function, as they contain a decrease in af

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

252 Together, the findings suggest ADCC is protective in the eye and that nonneutralizing a

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

254 d HIV-1 envelope glycoprotein (Env)-targeted ADCC were frequently identified in HIV-2-infected indivi

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

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

257 An increasing body of evidence suggests that ADCC contributes to protection against HIV-1 acquisition

258 The ADCC was analyzed by focal expansion assay and CD107 cyt

259 ts further identified distinctions among the ADCC assays.

260 (gB) and the pentameric complex (PC) and the ADCC response in HCMV-seropositive (R+) LTRs and in sero

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

262 (177)Lu-lilotomab-satetraxetan increased the ADCC induction to 30% +/- 3% of that in Raji cells, repr

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

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

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

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

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

268 atment, they contribute significantly to the ADCC-capable effector cell pool in patients on antiretro

269 ar, gB-specific Abs were associated with the ADCC response.

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

271 aluable information on how to stabilize this ADCC-vulnerable conformation.

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

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

274 nt susceptibility of HIV-1-infected cells to ADCC in regard to CD4 expression.

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

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

277 ral inoculum sensitizing uninfected cells to ADCC prior to de novo Env expression.

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

279 higher susceptibilities of infected cells to ADCC.

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

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

282 ects the susceptibility of infected cells to ADCC.

283 as been shown to sensitize infected cells to ADCC.

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

285 mation, thereby increasing susceptibility to ADCC.

286 nregulating CD4 could be more susceptible to ADCC than late-stage infected cells that have fully down

287 ent and leaves infected cells susceptible to ADCC.

288 infected cells, rendering them vulnerable to ADCC responses.

289 ediate antibody-dependent cellular toxicity (ADCC), for a preclinical assessment of immunotherapy of

290 ug sensitivity by exploiting TAMs to trigger ADCC.

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

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

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

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

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

296 individuals are needed to determine whether ADCC has a role in preventing KS.

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

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

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

300 e role in other herpesvirus infections; yet, ADCC has never been investigated in the context of KSHV