ライフサイエンスコーパス: killing by

1 strains that bind C4BP require properdin for killing by 2C7, whereas strains that do not bind C4BP ar

2 eased C. muridarum susceptibility to vaginal killing by ~8 times.

3 mplement, eosinophils greatly increased cell killing by a complement-dependent cell-mediated cytotoxi

4 killing by apolactoferrin but did not block killing by a lactoferrin-derived peptide.

5 y (P<0.05) decreased intracellular bacterial killing by a mouse alveolar macrophage cell line and pri

6 G mutants, in turn, correlated with enhanced killing by a range of CAPs of diverse structure and orig

7 making them susceptible to phagocytosis and killing by a secondary phagocyte.

8 ntly increased capacity to mediate bacterial killing by abundant production of reactive oxygen specie

9 ome of these strains avoid contact-dependent killing by accumulating immunity genes to effectors that

10 d with the ability of the strains to survive killing by acid and oxidative agents.

11 s, those lacking OprD were more resistant to killing by acidic pH or normal human serum and had incre

12 or the DR5 agonistic antibody AMG655 or cell killing by activated T cells.

13 onal Mycobacterium bovis BCG mutant enhanced killing by ADEP unlike in other bacteria.

14 but similar to PBNs, the enhanced bacterial killing by AINs accompanied both better granule maturati

15 The results provide an insight into assisted killing by an exogenous alkene with dark toxicity effect

16 al antiserum modestly increased phagocytosis/killing by an oxidative burst of murine neutrophils in v

17 B, C, W, and Y capsules limited CP-mediated killing by anti-fHbp, the unencapsulated group A mutant

18 of Hia, which facilitated their escape from killing by anti-Hia antisera.

19 results in longer time needed for bacterial killing by antibiotic treatment and shows evidence of be

20 with CF and measured their susceptibility to killing by antibiotics and host defenses.

21 Dormant persister cells that are tolerant to killing by antibiotics are responsible for this apparent

22 ow a small fraction of microbes that resists killing by antibiotics can emerge in a population of gen

23 ants of bacterial cells that are tolerant to killing by antibiotics(1).

24 , most importantly, is highly susceptible to killing by antibiotics, showing that endogenous oxidativ

25 ted targets also increased susceptibility to killing by antibiotics.

26 a infection promotes S. aureus resistance to killing by antibiotics.

27 on a plasmid were all susceptible to opsonic killing by antibodies to PNAG.

28 ability of gram-negative bacteria to resist killing by antimicrobial agents and to avoid detection b

29 n, DNA binding by BrlR, and recalcitrance to killing by antimicrobial agents of DeltasagS biofilm cel

30 taining 2-O-sulfate motifs inhibit S. aureus killing by antimicrobial factors secreted by degranulate

31 Haemophilus ducreyi resists killing by antimicrobial peptides encountered during hum

32 acterial replication and decreased bacterial killing by antimicrobial peptides.

33 ation by T-cell responses and to avoid rapid killing by antimycobacterial drugs.

34 erine protease inhibitors were able to block killing by apolactoferrin but did not block killing by a

35 MIC but not the recalcitrance of biofilms to killing by bactericidal agents.

36 Bacteria can withstand killing by bactericidal antibiotics through phenotypic c

37 ored biofilm resistance and recalcitrance to killing by bactericidal antibiotics to wild-type levels.

38 eliminated the recalcitrance of biofilms to killing by bactericidal antimicrobial agents, a phenotyp

39 l conditions for L-form growth and non-lytic killing by beta-lactam antibiotics.

40 The lack of meningococci killing by blood containing eculizumab resulted from inh

41 Many microbial cells are highly sensitive to killing by blue light (400-470 nm) due to accumulation o

42 even though the sifA mutant was sensitive to killing by bone marrow-derived macrophages from BALB/c.D

43 mpanzees in 15 communities and one suspected killing by bonobos.

44 When killing by bortezomib (an agent whose cytotoxicity in Ju

45 eptide at 0.1 nM are completely resistant to killing by C. albicans The peptide also protects macroph

46 nificant increase in the level of macrophage killing by C. albicans.

47 gest a therapeutic approach to mitigate cell killing by C. difficile toxins A and B.

48 s, but deleting arnT decreased resistance to killing by cationic antimicrobial peptides, such as poly

49 at likely permitted CD22(+) cell escape from killing by CD22-CAR T cells.

50 Here, we show that suppression of CTL killing by CD4(+)CD25(+)Foxp3(+) regulatory T cell (Treg

51 eath, Bax(-/-)Bak(-/-) DCs were resistant to killing by CD4(+)Foxp3(+) T regulatory cells (Tregs) com

52 fine mechanisms of pathogen recognition and killing by CD8(+) T cells.

53 reactive epitopes to escape recognition and killing by CD8+ T cells.

54 t affect WLBU2 killing compared to decreased killing by cefazolin.

55 We found a significant decrease in bacterial killing by CF alveolar macrophages compared with control

56 ocuses on three different mechanisms of cell killing by checkpoint kinase I inhibitors (CHK1i).

57 replication rate, total tumor population, or killing by chemotherapy of mouse or human leukemia cells

58 reviously proposed adaptive explanations for killing by chimpanzees, whereas the human impact hypothe

59 = 58 observed, 41 inferred, and 53 suspected killings) by chimpanzees in 15 communities and one suspe

60 ide (LPS) synthesis as uniquely required for killing by colicin N, but not by other colicins.

61 This renders the organism resistant to killing by complement in normal human serum.

62 es showed that both were resistant to direct killing by complement, although B. thailandensis acquire

63 acteremia because of their ability to resist killing by complement.

64 Enhanced bacterial killing by CPPD-induced NETs demonstrates their ability

65 aberrant growth and was more susceptible to killing by crystal violet, osmotic shock, and select car

66 agy control cancer-cell-intrinsic evasion of killing by CTLs and we highlight the importance of these

67 ion augmented pore formation by perforin and killing by CTLs.

68 te to phenotypes associated with escape from killing by CTLs.

69 oth granzyme B- and Fas-mediated pathways of killing by CTLs; however, the kinetics of caspase activa

70 ll surface, PDHc is an important mediator of killing by CXCL10.

71 e myeloid leukemia (AML) cells for cytotoxic killing by cytarabine (Ara-C).

72 y-state levels, leaving cells susceptible to killing by cytotoxic agents normally exported by MRP1.

73 cells were significantly more susceptible to killing by cytotoxic chemotherapy following androgen dep

74 ng schemes optimized to sustain and maximize killing by cytotoxic immune effector systems.

75 tibility class I (MHC-I) expression to evade killing by cytotoxic T lymphocytes (CTLs).

76 equent PD-L1 upregulation protects them from killing by cytotoxic T lymphocytes, yet dampens the anti

77 lsion, renders E. faecalis more resistant to killing by defensins and less susceptible to focal targe

78 Antibodies to TNF-alpha reversed the 95% killing by Deltaisp2/isp3, whereas they grew normally in

79 system, GraRS, is involved in resistance to killing by distinct host defense cationic antimicrobial

80 ntly in human cancers, confers resistance to killing by DNA-damaging agents.

81 L4A and GET4 proteins and resistance to cell killing by DNA-damaging agents.

82 e pathways to predict cellular resistance to killing by DNA-damaging agents.

83 A repair and sensitizes transformed cells to killing by DNA-damaging drugs.

84 ht to enhance the potency and specificity of killing by driving lytic granule fusion at the synapse a

85 is phenomenon enables the bacteria to escape killing by drugs and is presumed to be, at least partly,

86 the impact of EGFR expression on tumor cell killing by EGFR mAb.

87 tinib with obatoclax caused synergistic cell killing by eliciting autophagic cell death that was depe

88 response, participating directly in parasite killing by encapsulating and clearing the infection.

89 e a promising strategy to improve tumor cell killing by enhancing the interaction between humoral and

90 protecting M. catarrhalis from intracellular killing by epithelial cells.

91 ts of Escherichia coli are hypersensitive to killing by exogenous cytidine, adenosine, or guanosine,

92 cellular H2O2 threshold to enable more rapid killing by exogenous sources of H2O2.

93 oncentration of CD11b blocking Ab, S. aureus killing by female BMN was greatly reduced compared with

94 etic targets that can sensitize AML cells to killing by FLT3 inhibitors, we performed a genome-wide R

95 t MHC-I downregulation did not promote rapid killing by freshly isolated CD8(+) T cells.

96 ulation plays a critical role in target cell killing by freshly isolated human CD8(+) T cells, which

97 sensitized NDM-1-producing K. pneumoniae to killing by freshly isolated human neutrophils, platelets

98 udged from flow cytometric assays, bacterial killing by GA occurred within minutes.

99 Efficient killing by GA was also demonstrated in Acinetobacter bau

100 ants of Gal3-binding sugar moieties, escaped killing by Gal3.

101 ormal and cancer stem cells are resistant to killing by genotoxins, but the mechanism for this resist

102 ich were found to be important for resisting killing by H(2)O(2) Finally, DeltamumR exhibited reduced

103 utant were more sensitive than the parent to killing by H2O2.

104 olated an ALL cell line that is resistant to killing by HA22.

105 sceptibility of NC101 and NC101DeltagadAB to killing by host antimicrobial peptides and their translo

106 edly increased the resistance of bacteria to killing by host defenses and antibiotics, and reduced th

107 tion plays in circumventing detection and/or killing by host defenses.

108 odalis glossinidius, requires PhoP to resist killing by host derived antimicrobial peptides.

109 of adenosine in sPLA2-IIA-mediated S. aureus killing by host is still unknown.

110 ed to RAG hosts suggesting that avoidance of killing by host NK cells might be essential for autoanti

111 s, and resistance to bacterial ingestion and killing by host phagocytes.

112 lement evasion that allows for resistance to killing by human complement and persistence in mice.

113 ement pathways, T. forsythia is resistant to killing by human complement, which is present at up to 7

114 ensitive than the wild-type parent strain to killing by human lysozyme in the presence of human apola

115 least 2-fold more resistant to SP-A-mediated killing by human macrophages than their respective early

116 ptides, which correlated with increased MRSA killing by human neutrophils and within neutrophil extra

117 rain from oxidative stress in vitro and from killing by human neutrophils ex vivo.

118 mutant was also more susceptible than BG2 to killing by human neutrophils in vitro.

119 related with higher resistance to nonopsonic killing by human neutrophils in vitro.

120 eumoniae has enhanced capacity to circumvent killing by human neutrophils, the primary cellular defen

121 enhanced the susceptibility of S. aureus to killing by human neutrophils.

122 fluence complement-mediated opsonophagocytic killing by human neutrophils.

123 ex vivo, which was associated with increased killing by human neutrophils.

124 nt C3 on these bacteria for opsonophagocytic killing by human neutrophils.

125 Differences in sensitivity to killing by human nLc4 LOS IgG may account for the fact t

126 Correspondingly, IL-21 induced MRSA killing by human peripheral blood neutrophils.

127 ant was more susceptible to phagocytosis and killing by human polymorphonuclear cells (P = 0.01 and P

128 tant strain is more susceptible to oxidative killing by human polymorphonuclear leukocytes and displa

129 his toxin gene region increase resistance to killing by human polymorphonuclear leukocytes, increase

130 is severely attenuated in ability to resist killing by human polymorphonuclear leukocytes.

131 nt mutants demonstrate reduced resistance to killing by human serum.

132 st vertebrates are most threatened by direct killing by humans.

133 HSV-1 was found to be more sensitive to killing by hydrogen peroxide in the presence of a catala

134 hyloxanthin production and susceptibility to killing by hydrogen peroxide, respectively.

135 g that the luxS mutant was more sensitive to killing by hydrogen peroxide, suggesting a potential req

136 oxidative PMN-mediated killing and oxidative killing by hydrogen peroxide.

137 ptibility of both bacterial species to rapid killing by immune cells and can improve bacterial cleara

138 rium is able to resist antimicrobial peptide killing by induction of the PhoP-PhoQ and PmrA-PmrB two-

139 confirmed a role for PorB2 in resistance to killing by infant rat serum.

140 ne B4 (LTB4), which are involved in parasite killing by infected macrophages.

141 Chi3l1 augments macrophage bacterial killing by inhibiting caspase-1-dependent macrophage pyr

142 echanisms by which bacterial pathogens avoid killing by innate host responses, including autophagy pa

143 s, the esx-3 region, in evasion of bacterial killing by innate immunity.

144 Rapid parasite killing by intravenous artesunate might obscure the effe

145 ans, its absence sensitizes the bacterium to killing by ionizing radiation (IR).

146 thracis, which is known to escape phagocytic killing by its pXO2 encoded poly-d-gamma-glutamic acid (

147 in 3 (Prdx3) that render them susceptible to killing by K-Ras(G12V)-mediated ROS production.

148 atically identify host factors that regulate killing by L. pneumophila.

149 ial function plays an essential role in cell killing by lapatinib and obatoclax, as well as radiosens

150 ducing enzymes were used to assess bacterial killing by leukocytes.

151 est (BIAT)) for investigating illegal badger killing by livestock farmers across Wales.

152 greater sensitivity than the sapA mutant to killing by LL-37.

153 cterial burdens and more efficient bacterial killing by Ly6B.2(+) myeloid cells and macrophages compa

154 the cellular mechanism through which failed killing by lymphocytes causes systemic inflammation invo

155 ed and displayed increased susceptibility to killing by lysosomal SF and the antimicrobial peptide LL

156 chanisms which B. subtilis utilizes to avoid killing by lysozyme.

157 We observed 100% complement-dependent killing by mAb 2C7 of a mutant that expressed lactose (G

158 ered effective FcalphaRI-mediated tumor cell killing by macrophages already at low effector to target

159 CaGPI15 mutant is more susceptible to killing by macrophages and epithelial cells and has redu

160 sitive phenotype and was more susceptible to killing by macrophages than the WT strain.

161 part arise from increased susceptibility to killing by macrophages, as well as by other phagocytes s

162 gnaling protects through enhancing bacterial killing by macrophages, which is independent of the infl

163 acting in part via a modulation of bacterial killing by macrophages.

164 y tandem repeats are relatively resistant to killing by macrophages.

165 of infection by opsonization, ingestion, and killing by macrophages.

166 ve the capacity to evade DC (and macrophage) killing by manipulation of autophagic pathways.

167 N-gamma sensitizes these leukemias to T cell killing by mechanisms other than MHC upregulation.

168 nvironment may impair NK-mediated tumor cell killing by mechanisms that are not fully understood.

169 anner which affects MIC and recalcitrance to killing by microbicidal antimicrobial agents.

170 he MICs and the recalcitrance of biofilms to killing by microbicidal antimicrobial agents.

171 We found that H. pylori is resistant to killing by millimolar concentrations of HOCl and respond

172 p53 inhibition boosts bacterial killing by mouse neutrophils and oxidant generation by h

173 ch in turn leads to a reduction in bacterial killing by moxifloxacin, a substrate of the NorB efflux

174 Bacterial killing by MSC was found to be mediated in part by secre

175 CD11b reduced both ROS levels and S. aureus killing by murine BMN from both sexes.

176 tein, is required for Mtuberculosis to evade killing by NADPH oxidase and LAP.

177 ha resulted in their increased resistance to killing by natural cytotoxic cells.

178 Killing by NET-forming cells is ascribed to these struct

179 nables N. gonorrhoeae to escape trapping and killing by NETs during symptomatic infection, highlighti

180 n and biofilm formation, decreases bacterial killing by neutrophil extracellular traps, and modulates

181 ies showed significantly enhanced uptake and killing by neutrophils after critical levels of C3 were

182 oxidative stress, febrile temperatures, and killing by neutrophils and also had defects in filamenta

183 ggregatibacter actinomycetemcomitans resists killing by neutrophils and is inhibited by azithromycin

184 virulence and making it less susceptible to killing by neutrophils and more capable of causing invas

185 criptional regulator of genes directing AP53 killing by neutrophils and regulates the levels of the r

186 ous M1 protein rescues M1-deficient GAS from killing by neutrophils and within neutrophil extracellul

187 MPO) is important in intracellular microbial killing by neutrophils but extracellularly causes tissue

188 ion rather than on enhanced opsonophagocytic killing by neutrophils or protection against toxin-media

189 oxygen species, and intracellular bacterial killing by neutrophils remains intact.

190 but does not affect intracellular phagocytic killing by neutrophils.

191 degrades NETs to help N. gonorrhoeae resist killing by neutrophils.

192 e extent of S. aureus opsonophagocytosis and killing by neutrophils.

193 s, and phagocytosis, and succeeds in evading killing by neutrophils.

194 reased susceptibility to complement-mediated killing by neutrophils.

195 B-negative staphylococci more susceptible to killing by neutrophils.

196 veloped strategies to evade phagocytosis and killing by neutrophils.

197 e the ability of S. aureus biofilms to evade killing by neutrophils.

198 o a secondary stimulus, preventing oxidative killing by neutrophils.

199 fied by Tn-seq in A. baumannii resistance to killing by NHS but not by normal mouse serum, highlighti

200 C4b deposition, and increased resistance to killing by NHS.

201 tion of C4b, and increased susceptibility to killing by NHS.

202 Killing by NK cells is mediated by a small family of act

203 Ex vivo and in vivo tumor cell killing by NK cells were significantly reduced in surgic

204 g receptor 2B4, thereby leading to decreased killing by NK cells.

205 well as Fas/Fas ligand-dependent pathways of killing by NK cells.

206 cer cells more susceptible to NKG2D-mediated killing by NK cells.

207 solated from the same individual escape cell killing by NK cells.

208 apy, suggesting a decrease in TRAIL-mediated killing by NK cells.

209 owing T. spiralis larvae were susceptible to killing by NO in vitro, whereas mature larvae were highl

210 levant A. baumannii strains are resistant to killing by normal human serum (NHS), an observation supp

211 eptibility of an lptA null strain of FA19 to killing by normal human serum (NHS).

212 correlated with enhanced protection against killing by normal human serum.

213 ased microbial ROS production can potentiate killing by oxidants and antibiotics.

214 guinis protects Drosophila melanogaster from killing by P. aeruginosa in a nitrite-dependent manner.

215 T6SS), and prevents T6SS-dependent bacterial killing by P. aeruginosa.

216 elegans and human lung epithelial cells from killing by P. aeruginosa.

217 macrophage pyroptosis, attenuated both cell killing by p30 in a 293T transient overexpression system

218 It is, therefore, apparent that cell killing by PAF26 is complex and unusually dependent on e

219 es not induce serotype 3 (ST3) S. pneumoniae killing by phagocytes in vitro, protects mice from death

220 ing cytokine levels, promoting extracellular killing by phagocytes, and generating a granulomatous re

221 ram-negative bacteria and supports bacterial killing by phagocytes.

222 ella by directly coating bacteria to promote killing by phagocytes.

223 We confirmed the cell shape-specific killing by photothermal colloid antibodies in a mixture

224 in MICs tracked with increased resistance to killing by platelet-derived but not neutrophil-derived H

225 g Gram-negative pathogen in CGD that resists killing by PMN of CGD patients (CGD PMN) and inhibits PM

226 B. parapertussis is able to avoid bacterial killing by polymorphonuclear leukocytes (PMN) if specifi

227 ested whether PGE(2) could inhibit bacterial killing by polymorphonuclear neutrophils (PMN) using a m

228 ast cancer and melanoma cells susceptible to killing by PR1-specific CTLs (PR1-CTL) and the anti-PR1/

229 TDE0471 protects T.denticola from serum killing by preventing the deposition of membrane attack

230 Therefore, we examined phagocytic killing by primary human monocytes and monocyte-derived

231 not cytotoxic) dramatically increased their killing by proteasome inhibitors and inhibitors of ubiqu

232 -induced apoptosis and no protection against killing by Puma or ABT-737 plus Noxa overexpression.

233 an neutrophils susceptible to LukAB-mediated killing by purified LukAB as well as during S. aureus in

234 is usually resists complement-mediated serum killing by recruiting to its surface a complement inhibi

235 ction and triple-negative breast cancer cell killing by reovirus.

236 ibiotics, P. gingivalis can evade antibiotic killing by residing within gingival keratinocytes.

237 ith mutations of phoPQ are hypersensitive to killing by RNS generated in vitro.

238 ated resistance of NTHi to antibody-directed killing by serum complement.

239 Resistance to killing by serum enhances the capacity of Klebsiella pne

240 G. bethesdensis resists killing by serum, CGD polymorphonuclear leukocytes (PMN)

241 esponsible for preventing activation of, and killing by, serum complement could inform new approaches

242 face sialyl Lewis X (sLe(X)) exacerbates the killing by several wild-type IAV strains and a previousl

243 that mitochondrial damage and ROS drive cell killing by SFB, while glycolytic cell reprogramming may

244 in protecting SIV-infected macrophages from killing by SIV-specific CD8(+) T cells.

245 ote, this binding was required for bacterial killing by sphingosine, as revealed by genetic experimen

246 linical GBS isolates are highly sensitive to killing by sPLA2-IIA but not by human antimicrobial pept

247 erminating spores become more susceptible to killing by stressors, induction of germination has been

248 potently and specifically inhibit S. aureus killing by synthetic CRAMP.

249 n endothelium increased immune-mediated cell killing by T cells and natural killer (NK) cells, thereb

250 vivo because of inefficient recognition and killing by T cells.

251 nity proteins that render protection against killing by T6SS predatory cells.

252 in cancer treatment has been to trigger cell killing by targeting microtubule dynamics or spindle ass

253 ngly suggest that Spiroplasma initiates male killing by targeting the dosage compensation machinery d

254 ion mutant of MG_427 was highly sensitive to killing by tert-butyl hydroperoxide and H2O2 compared to

255 portant contributor to periodontitis, evades killing by the alternative complement cascade by binding

256 genic biofilms, markedly enhancing bacterial killing by the antimicrobial agent (3-log increase versu

257 ureus biofilms showed less susceptibility to killing by the antimicrobial peptide LL-37 when compared

258 37 and increased bacterial susceptibility to killing by the antimicrobial peptide.

259 class I C/E16 were highly susceptible to the killing by the CD8alphaalpha(+) AP-NK cell.

260 ain FA19 results in increased sensitivity to killing by the classical pathway of complement.

261 Evasion of killing by the complement system, a crucial part of inna

262 toaggregation and protects the pathogen from killing by the complement system.

263 he RecQ helicase Blm are highly sensitive to killing by the DNA replication stressor hydroxyurea.

264 and enhances the susceptibility of NC101 to killing by the host antimicrobial peptide cryptdin-4 but

265 d several ways to protect themselves against killing by the host complement system.

266 ormed less biofilm and was less resistant to killing by the host complement.

267 gies to escape innate immune recognition and killing by the host.

268 Higher IFN-beta levels in vivo increase GBS killing by the host.

269 lar insights into MAC assembly and bacterial killing by the immune system.

270 , forming drug-tolerant biofilms that resist killing by the immune system.

271 These include enhancing bacterial killing by the innate immune system.

272 LA class II and restored recognition but not killing by the LANA-specific clones.

273 conditions, including antibiotic stress and killing by the mouse-derived macrophage cell line J774.

274 ctively, more susceptible than the parent to killing by the neutrophil cell line HL-60 cells.

275 es lacking pAKT (P = .024) and exceeded cell killing by the PI3K-delta-specific inhibitor idelalisib.

276 Many human cancer cells are sensitive to killing by the proapoptotic ligand TNF-related apoptosis

277 R system, thereby defending the cell against killing by the Sn1-type methylating agent.

278 Killing by the T6SS results from repetitive delivery of

279 lls, dendritic cell (DCs) are susceptible to killing by these activated T cells that involve perforin

280 tibacterials, leading to the hypothesis that killing by these agents can involve ROS-mediated self-de

281 air and checkpoint signaling pathways affect killing by these agents individually and in combination.

282 that contributes to effective DNA damage and killing by these agents.

283 a trophozoites were found to be resistant to killing by these antimicrobial peptides, and LL-37 and C

284 Perforin-mediated killing by these densely granulated NK cells was essenti

285 Through synergistic cell killing by these distinct reactive oxygen species, W(18)

286 with decreased metabolic rate, refractory to killing by these drugs, and able to generate drug-resist

287 t the dividing cells are more susceptible to killing by tobramycin and ciprofloxacin.

288 th rMIF is associated with reduced bacterial killing by tobramycin.

289 Acquisition of androgen-independent killing by TPA correlates with activation of p38(MAPK),

290 n MIC of 1 mg/L exhibited significantly less killing by tPMP, compared with strains with an MIC of </

291 bacterial and anticancer drugs initiate cell killing by trapping the covalent complexes formed by top

292 nd apoptosis in vivo and increased bacterial killing by treated cells.

293 TF combinations that potentiated antibiotic killing by up to 10(6)-fold and delivered these combinat

294 FANCJ-deficient cells are not sensitive to killing by UV irradiation, yet we find that DNA mutation

295 XP cells are hypersensitive to killing by UV radiation, and XP cancers have characteris

296 Resistance to killing by Verde2, by means of alterations in host surfa

297 for T6SS-mediated secretion and target cell killing by Vibrio cholerae and Acinetobacter baylyi.

298 ile M. tuberculosis is highly susceptible to killing by vitamin C, other Gram-positive and Gram-negat

299 In the presence of erythrocytes, bacterial killing by VPO1 is slightly reduced.

300 Susceptibility of HNSCC lines to killing by VSV varied.