ライフサイエンスコーパス: phagosomal

1 -killed Escherichia coli, demonstrating that phagosomal acidification affects endosomal receptor-medi

2 ic fibrosis lung disease involving defective phagosomal acidification and bacterial killing in alveol

3 d not affect POS internalization but reduced phagosomal acidification and delayed POS protein clearan

4 luating bacterial intracellular survival and phagosomal acidification and maturation and by testing t

5 TFEB promoted phagosomal acidification and protein degradation.

6 oxidase NOX2 in DCs, which in turn inhibited phagosomal acidification and reduced the degradation of

7 Critical to phagosomal acidification are various channels derived fr

8 summary, our results identify the control of phagosomal acidification as a novel function of Abl tyro

9 Phagosomal acidification began within 3 min of zymosan b

10 Inhibition of phagosomal acidification blocks TLR9 accumulation on pha

11 Importantly, blocking of phagosomal acidification by inhibiting vacuolar-type H(+

12 Phagosomal acidification facilitates the optimal functio

13 ng fluorescent probe that enabled imaging of phagosomal acidification in activated macrophages.

14 associated with accelerated phagocytosis and phagosomal acidification in DCs.

15 We also measured the kinetics of phagosomal acidification in J774A.1 and murine alveolar

16 The rate of phagosomal acidification in J774A.1 cells was not slowed

17 Differences in phagosomal acidification indicated that in chicken lungs

18 d NALP3 activation, and inhibition of either phagosomal acidification or cathepsin B activity impaire

19 orbidden ordinal patterns, implying that the phagosomal acidification process was a stochastic dynami

20 Inhibition of macrophage phagosomal acidification resulted in a 30-fold reduction

21 phage viability and found that inhibitors of phagosomal acidification significantly impaired USA300 i

22 In addition, inhibition of phagosomal acidification significantly improved iscl(-)

23 crophages to produce cytokines is due to the phagosomal acidification that disrupts endosomal ligand-

24 Thus, human Mphi do not require phagosomal acidification to kill and degrade Hc yeasts,

25 Phagosomal acidification was crucial for O(2) (*-) perme

26 was regulated during DC maturation and that phagosomal acidification was impaired in DCs in which th

27 ly blocked by bafilomycin A, an inhibitor of phagosomal acidification.

28 culosis has multiple mechanisms of resisting phagosomal acidification.

29 umulation of PtdIns4P is required for proper phagosomal acidification.

30 n be rescued bypharmacological inhibition of phagosomal acidification.

31 target the host vacuolar ATPase to withstand phagosomal acidity, the MgtC protein acts on Salmonella'

32 Thus, a v-ATPase-dependent phagosomal activation of Cat D was required for the gene

33 ession nor Ag uptake, but rather to impaired phagosomal Ag degradation.

34 While investigating the requirement for phagosomal alkalinization in the host defense against pu

35 phagosome, this permeabilization results in phagosomal and cytoplasmic mixing and allows extracellul

36 DNA-based probes that ratiometrically report phagosomal and endosomal NO, and can be molecularly prog

37 psin D-positive lysosomes, without mixing of phagosomal and lysosomal contents.

38 polyreactive Ig and complement in directing phagosomal antigen processing for cross-presentation.

39 g the host and bacterial factors that affect phagosomal antigen processing may help facilitate new st

40 Interestingly, the phagosomal association of sortilin is critical for the d

41 Phagosomal autonomy could serve as a basis for the intra

42 fication of phagosomes and the processing of phagosomal bacterial nucleic acids and was required for

43 tments within the same cell is determined by phagosomal cargo and may affect the outcome of antigen p

44 Specific ligands present in the phagosomal cargo influence the rate of phagosome fusion

45 idence indicates that receptor engagement by phagosomal cargo, as well as inflammatory mediators and

46 Mtb specifically under conditions that mimic phagosomal cation concentrations, and further support a

47 We propose that CFTR transiently increases phagosomal chloride concentration after infection, poten

48 contact of Rab5a-positive vesicles with the phagosomal coat.

49 hagosome contact by binding to PI(3)P in the phagosomal coat.

50 Phagosomal compaction, a crucial step in phagolysosome m

51 e, as it directly inhibits maturation of the phagosomal compartment in which the bacterium is taken u

52 thogen Listeria monocytogenes escapes from a phagosomal compartment into the cytosol by secreting the

53 osis, and then actively invade from within a phagosomal compartment to form a parasitophorous vacuole

54 oxide radical (O(2) (*-)) is produced at the phagosomal compartment toward the internalized parasite

55 form an activation-induced Rab7(+) endosomal/phagosomal compartment.

56 mice exhibit decreased copper transport into phagosomal compartments and a reduced ability to kill Sa

57 Cs to CD4(+) T cells in the endosomal versus phagosomal compartments of Ms versus DCs.

58 ns indicate that the composition of distinct phagosomal compartments within the same cell is determin

59 ages, where M. tuberculosis resides in early-phagosomal compartments, in MSCs the majority of bacilli

60 y using liposomal model membranes that mimic phagosomal compartments.

61 i to vesicles that partially overlapped with phagosomal compartments.

62 phagosome maturation and trafficked to late phagosomal compartments.

63 lysosome formation and that USA300 may sense phagosomal conditions and upregulate expression of a key

64 and maturation and by testing the impact of phagosomal conditions on bacterial viability.

65 Macrophages sample the phagosomal content and orchestrate the innate immune res

66 tion', which leads to the degradation of the phagosomal content.

67 This allows escape of phagosomal contents into the cytosol, where they access

68 Ctr1) and ATP7A, a transporter implicated in phagosomal Cu compartmentalization, respectively.

69 l recruitment of YFP-tagged p67(phox) to the phagosomal cup, and, after phagosome internalization, a

70 get particle, is transiently enriched in the phagosomal cup.

71 accumulated at extending pseudopodia and in phagosomal cups in trophozoites exposed to erythrocytes

72 nd actin rearrangements for engulfment; have phagosomal cysteine proteases active at low pH; and can

73 The generation of phagosomal cytotoxic reactive species (i.e., free radica

74 ich activates SYK and NADPH oxidase to cause phagosomal damage even when spliced into a heterologous

75 environment accidentally, for example, upon phagosomal damage, whereas pathogens routinely accessing

76 gosome, whereas enhancing HIF-1alpha reduced phagosomal decoration.

77 ies used by bacteria to resist antimicrobial phagosomal defenses and transiently pass through this co

78 by which the bacteria might evade macrophage phagosomal defenses are unclear.

79 is more sensitive to lysozyme, we show that phagosomal degradation and release of intracellular liga

80 mes and become acidified before the onset of phagosomal disruption.

81 particles confirmed a major role for GILT in phagosomal disulfide reduction in both resting and inter

82 Assessment of phagosomal disulfide reduction upon internalization of I

83 , and Beclin-1) and augmented recruitment of phagosomal (EEA1 and Rab7) and lysosomal (LAMP1) protein

84 Thus, phagosomal/endosomal binding of peptides locally generat

85 s that the depletion of Mg(2+) observed upon phagosomal engulfment may act to trigger isoTb biosynthe

86 ism that triggers edaxadiene production upon phagosomal engulfment.

87 mably, isoTb production should be induced by phagosomal entry.

88 sis is its ability to escape the destructive phagosomal environment and inhibit the host cell respira

89 sured the shear modulus and viscosity of the phagosomal environment concurrently with the phagosomal

90 her intracellular pathogens that control the phagosomal environment use specialized protein export sy

91 ze cytosolic and phagosomal pH, and regulate phagosomal enzymatic activities.

92 Furthermore, activation of a phagosomal enzyme, inducible nitric oxide synthase, whic

93 (LLO) is a pore-forming toxin that mediates phagosomal escape and cell-to-cell spread of the intrace

94 tion significantly delayed but did not block phagosomal escape and cytosolic replication, indicating

95 ve and proliferate within phagocytes through phagosomal escape and cytosolic replication.

96 gh an intracellular life cycle that includes phagosomal escape and extensive proliferation within the

97 e production in the early FCP and restricted phagosomal escape and intracellular growth in an NADPH o

98 enicity island (FPI) mutant, is deficient in phagosomal escape and intracellular growth, whereas F. n

99 ied IgG enhanced phagocytosis but restricted phagosomal escape and intracellular proliferation.

100 ia through phagocytic pathways that restrict phagosomal escape and intracellular proliferation.

101 ing phagosome (FCP) is important for optimal phagosomal escape and subsequent intracellular growth.

102 hagosomal maturation is required for optimal phagosomal escape and that the early FCP provides cues o

103 variety of acid phosphatases, whose roles in phagosomal escape and virulence have been documented yet

104 s than wild-type Schu S4 and were capable of phagosomal escape but exhibited reduced intracellular gr

105 Addition of biotin complemented the phagosomal escape defect of the FTN_0818 mutant, demonst

106 f endosomal acidification mimicked the early phagosomal escape defects caused by mutation of the FPI-

107 The key role of biotin in phagosomal escape implies biotin may be a limiting facto

108 Phagosomal escape is a multistep process characterized b

109 The contribution of host factors to Listeria phagosomal escape is incompletely defined.

110 unaffected, suggesting that ESX-1-dependent phagosomal escape is not required for CD8(+) T-cell prim

111 Recent studies indicate that phagosomal escape may have a major impact on the nature

112 that a bacterial metabolite is required for phagosomal escape of an intracellular pathogen, providin

113 thermore, HD5 neither inhibited nor enhanced phagosomal escape of Shigella Collectively, these findin

114 rence, invasion, intracellular survival, and phagosomal escape of the bipC mutant.

115 acpA, acpB, and acpC deletions affected the phagosomal escape or cytosolic growth of Schu S4 in muri

116 The mechanism underlying rickettsial phagosomal escape remains unknown, although the genomic

117 include cellular uptake and internalization, phagosomal escape, and intracellular cargo concentration

118 this interlacing is essential to secretion, phagosomal escape, and intracellular replication.

119 malarial drug, inhibits Burkholderia growth, phagosomal escape, and subsequent MNGC formation.

120 orted to play important roles in Francisella phagosomal escape, inhibition of the respiratory burst,

121 e precisely regulated in order to facilitate phagosomal escape, intracellular growth, and cell-to-cel

122 VgrG and IglI are required for F. tularensis phagosomal escape, intramacrophage growth, inflammasome

123 These results reveal a crucial role for phagosomal escape, not for delivery of antigen to the cl

124 As with phagosomal escape, the F. tularensis Type VI Secretion S

125 la-containing phagosome (FCP) and restricted phagosomal escape, while FcgammaR-dependent phagocytosis

126 ults on the timing and extent of Francisella phagosomal escape.

127 olipase D activity, has been associated with phagosomal escape.

128 ltaFTT1103 mutant bacteria were defective in phagosomal escape.

129 brane protrusions, actin polymerization, and phagosomal escape.

130 regulated by bacterial genes associated with phagosomal escape.

131 III secretion apparatus (T3SA) in mediating phagosomal escape.

132 asmic pathogens, including Shigella, mediate phagosomal escape.

133 The phenomenon of "phagosomal extrusion" indicates the existence of a previ

134 dy was to assess the effect of GILT on major phagosomal functions with an emphasis on proteolytic eff

135 ii infects alveolar macrophages and promotes phagosomal fusion with autophagosomes and lysosomes, est

136 Phagosomal fusion with late endosomes and lysosomes enha

137 stinctive Zn sequestration strategy elevated phagosomal H(+) channel function and triggered reactive

138 The unusual kinetics of phagosomal HOCl production in CF neutrophils confirm a r

139 e to killing, which suggests the presence of phagosomal immune evasion molecules.

140 D4(+) T cells maintained during a persistent phagosomal infection progressively deteriorates.

141 CD4(+) T cells maintained during persistent phagosomal infection.

142 s play a critical role in protection against phagosomal infections.

143 Our data demonstrate that a phagosomal inflammatory response of microglia is leading

144 A phagosomal integrity assay and lysosome-associated membr

145 Slc11a1 encodes a phagosomal ion transporter, Nramp1, that affects resista

146 viable filamentous L. pneumophila to escape phagosomal killing in a length-dependent manner.

147 o-BCFAs enhance bacterial resistance against phagosomal killing in macrophages.

148 Mg(2+) (0.43 mM), shifting Mtb to media with phagosomal levels (0.1 mM) led to a significant ( approx

149 s to phagosomes and the acidification of the phagosomal lumen.

150 e ESX-1 system secretes proteins which cause phagosomal lysis within the macrophage via an unknown me

151 hat VirS plays an important role in blocking phagosomal-lysosomal fusions.

152 se of infection in both humans and mice, how phagosomal M. tuberculosis Ags are processed and present

153 iquitin-mediated autophagy pathway access to phagosomal M. tuberculosis.

154 This promoted phagosomal maturation (EEA-1/Lamp-3) and autophagy (LC3-

155 teract M. tuberculosis-induced inhibition of phagosomal maturation and promote host-induced autophagy

156 of M. tuberculosis correlates strongly with phagosomal maturation and that the inducible GFP express

157 and discovered WhiB3 as crucial mediator of phagosomal maturation arrest and acid resistance in M. t

158 Furthermore, we also performed a phagosomal maturation assay and observed that the activa

159 S. iniae does not alter neutrophil phagosomal maturation but instead is able to adapt to th

160 Pravastatin modulated phagosomal maturation characteristics in macrophages, ph

161 parable capacity for phagocytosis and normal phagosomal maturation compared to wild-type macrophages.

162 key aspects in phagocytic cup remodeling and phagosomal maturation could be influenced by target morp

163 YN-1 leads to common as well as differential phagosomal maturation defects.

164 inhibition of Rab7 acquisition and arrest of phagosomal maturation depends on Rab22a.

165 he data are consistent with a model in which phagosomal maturation events associated with the acquisi

166 gnition and triggering of Th17 responses, to phagosomal maturation has not been defined.

167 Mycobacterium tuberculosis arrests phagosomal maturation in infected macrophage, and, apart

168 culosis, edaxadiene, whose ability to arrest phagosomal maturation in isolation presumably contribute

169 We show that this block in phagosomal maturation is in part due to WhiB3-dependent

170 gether, these results demonstrate that early phagosomal maturation is required for optimal phagosomal

171 rophages phagocytose Mucor yeast, subsequent phagosomal maturation occurs, indicating host cells resp

172 ation of invading microbes by macrophages is phagosomal maturation through heterotypic endosomal fusi

173 induces inflammatory cytokines and controls phagosomal maturation through spleen tyrosine kinase act

174 hagocytic particle engulfment and subsequent phagosomal maturation to a degradative organelle.

175 r active TRIF signaling events, thus linking phagosomal maturation to specific TLR signaling pathways

176 Importantly, in the absence of MUNC13-4, phagosomal maturation was impaired as observed by the de

177 MUNC13-4 in selective vesicular trafficking, phagosomal maturation, and intracellular bacterial killi

178 ort that under certain conditions, including phagosomal maturation, possible actin depolymerization,

179 oss of functional Lyst leads to dysregulated phagosomal maturation, resulting in a failure to form an

180 METH interferes with phagocytic cells' phagosomal maturation, resulting in impaired fungal cont

181 In the process of blocking phagosomal maturation, the intracellular pathogen Mycoba

182 equire Dectin-1-dependent Syk activation for phagosomal maturation.

183 status of M. tuberculosis and the degree of phagosomal maturation.

184 phages and thereby controls phagocytosis and phagosomal maturation.

185 nd PX motif-containing proteins that promote phagosomal maturation.

186 pression of innate immune genes and blocking phagosomal maturation.

187 h many T4SS substrates being retained on the phagosomal membrane adjacent to the poles of the bacteri

188 ime after uptake, F. tularensis disrupts its phagosomal membrane and escapes into the cytoplasm.

189 ed listeriolysin O (LLO), which disrupts the phagosomal membrane and, thereby, allows the bacteria ac

190 " indicating that F. tularensis disrupts its phagosomal membrane by a mechanism that does not require

191 model and show that permeabilization of the phagosomal membrane does not require ESAT-6 secretion.

192 while activation of the NADPH oxidase at the phagosomal membrane generates reactive oxygen species wi

193 t lysosomes fuse with phagosomes to maintain phagosomal membrane integrity as the fungal pathogen Can

194 gering of TLR9 recruitment to the macrophage phagosomal membrane is a conserved feature of fungi of d

195 Penetration of the phagosomal membrane is initiated by the secreted haemoly

196 g and fusion of the virion envelope with the phagosomal membrane is likely facilitated by clustering

197 rastic spatial redistribution of TLR9 to the phagosomal membrane of A. fumigatus-containing phagosome

198 It also promotes phagosomal membrane permeabilization, allowing dsDNA and

199 m tuberculosis, induce type I IFNs following phagosomal membrane perturbations.

200 of-function mutations in Nramp1 (SLC11A1), a phagosomal membrane protein that controls iron export fr

201 que E3 ubiquitin ligase family important for phagosomal membrane remodeling by L. pneumophila.

202 oth PI4KIIalpha and PtdIns4P are detected on phagosomal membrane tubules.

203 gh the action of regulatory molecules on the phagosomal membrane.

204 of resting PMNs and was up-regulated to the phagosomal membrane.

205 iated reduction in cholesterol levels within phagosomal membranes counteract M. tuberculosis-induced

206 Endoplasmic reticulum (ER) contribution to phagosomal membranes is thought to provide antigen acces

207 ith dysfunctional recruitment of retromer to phagosomal membranes, reduced retromer levels, and impai

208 LLO mediates rupture of phagosomal membranes, thereby releasing bacteria into th

209 onfocal imaging and direct patch clamping of phagosomal membranes, we found that particle binding ind

210 that is rapidly synthesized and degraded on phagosomal membranes, where it recruits FYVE domain- and

211 the only kinase that produces PtdIns(3)P in phagosomal membranes.

212 CpG-containing compartments and A. fumigatus phagosomal membranes.

213 ed ratios of PI(3,4,5)P(3) to PI(3,4)P(2) on phagosomal membranes.

214 -3-phosphate (PI(3)P), which is generated in phagosomal membranes.

215 sion increased the duration of PtdIns(3)P on phagosomal membranes.

216 ce P(1B)-ATPases appear key to overcome high phagosomal metal levels and are required for the assembl

217 hagosome biogenesis and in adaptation to the phagosomal microenvironment.

218 al phagocytes generate ROS primarily via the phagosomal NADPH oxidase machinery.

219 By mapping phagosomal NO produced in microglia of live zebrafish br

220 itive phagosomes, concomitantly potentiating phagosomal NOX activity.

221 phate, a regulator of both NOX2 function and phagosomal or endosomal fusion.

222 ease recruits Mst1/2 from the cytosol to the phagosomal or mitochondrial membrane, with ROS subsequen

223 monella in vitro, in part due to inefficient phagosomal oxidant production, when compared with WT BMM

224 The phagosomal pathogen Leishmania appears unaffected by del

225 ssential for macrophage host defense against phagosomal pathogens, including Mycobacterium tuberculos

226 the ESX-1 type VII secretion system promotes phagosomal permeabilization and type I IFN production, k

227 we found that bafilomycin A did not prevent phagosomal permeabilization by F. tularensis LVS or viru

228 Here we show that phagosomal permeabilization mediated by the bacterial ES

229 eactive oxygen species (ROS), which regulate phagosomal pH and processing of particulate antigens for

230 n, BDCA1(+) and BDCA3(+) DCs display similar phagosomal pH and similar production of reactive oxygen

231 neutrophils occurs by neutralization of the phagosomal pH by NADPH oxidase.

232 regulator Cl- channel (CFTR) participates in phagosomal pH control and has bacterial killing capacity

233 Following phagocytosis, the phagosomal pH dropped rapidly to <6.5 in Ms but remained

234 capsulatum mutants that experience decreased phagosomal pH have not been identified.

235 Hence, chance in the final phagosomal pH introduces unpredictability to the outcome

236 ), we demonstrated that a modest decrease in phagosomal pH is sufficient to generate redox heterogene

237 Here, the neutralization of phagosomal pH reduces protease activity, which preserves

238 a Tmem176b-dependent cation current controls phagosomal pH, a critical parameter in cross-presentatio

239 membrane potentials, optimize cytosolic and phagosomal pH, and regulate phagosomal enzymatic activit

240 egments (POS), proteolysis of POS rhodopsin, phagosomal pH, phagosome fusion with early and late endo

241 otropic agent LysoTracker as an indicator of phagosomal pH, we obtained evidence that in the absence

242 phagosomal environment concurrently with the phagosomal pH.

243 trating that this response is independent of phagosomal pH.

244 These results support a model in which phagosomal PI3K generates PI(3,4,5)P(3) necessary for la

245 (DAG) was not generated uniformly across the phagosomal population, varying in a manner that directly

246 requires MyD88, Syk, and PI3K signaling and phagosomal processing to activate IRF1 and IRF3/IRF7 and

247 hat NOX2 activity not only affects levels of phagosomal proteolysis as previously shown, but also the

248 Phagosomal proteolysis of AM was assessed with fluorogen

249 WASH is required for efficient phagosomal proteolysis, and proteomic analysis demonstra

250 reactive oxygen species (ROS) production and phagosomal proteolysis.

251 Furthermore we observed a decrease in early phagosomal proteolytic efficiency in GILT-deficient macr

252 ve activation, driven by IL-4, modulated the phagosomal proteome to control macrophage function.

253 ps-34 completely abolishes the production of phagosomal PtdIns(3)P and disables phagosomes from recru

254 Remarkably, persistent appearance of phagosomal PtdIns(3)P, as a result of inactivating mtm-1

255 plays a novel and crucial role in producing phagosomal PtdIns(3)P.

256 idase response correlates with inhibition of phagosomal PtdIns3P accumulation and overlaps with the r

257 isappearance coincides with the emergence of phagosomal PtdIns3P.

258 phagosomes, little is known about how these phagosomal Rab proteins influence phagosome maturation.

259 ible factor 1 subunit alpha (HIF-1alpha) and phagosomal recruitment of mammalian target of rapamycin

260 cross-presentation requires Sec22b-mediated phagosomal recruitment of the peptide loading complex fr

261 monstrate that silica particles can generate phagosomal ROS independent of NOX activity, and we propo

262 and appeared in parallel with an increase in phagosomal ROS, as well as several hours later associate

263 cytosolic side of the plasma membrane after phagosomal rupture in infected macrophages.

264 at signals upon ligand engagement to promote phagosomal rupture.

265 ments of individual organelles indicate that phagosomal SHIP-1 enhances the early oxidative burst thr

266 Loss of the transporter Slc37a2 blocks phagosomal shrinkage, resulting in the expansion of the

267 ition of diverse ligands; in the case of Bb, phagosomal signaling involves a cooperative interaction

268 ntimicrobial hypochlorous acid (HOCl) in the phagosomal space.

269 Accessibility of iron at the phagosomal surface inside macrophage is crucial for surv

270 efficient removal of Lys63 linkages from the phagosomal surface.

271 microscopy shows that NDK-1 is expressed on phagosomal surfaces during cell corpse clearance in the

272 e found that these proteins were enriched on phagosomal surfaces through association with PtdIns(3)P

273 We propose that UNC-108 acts on phagosomal surfaces to promote phagosome maturation and

274 tiator, to strengthen DYN-1's association to phagosomal surfaces, and facilitates the maintenance of

275 transient enrichment of the RAB-5 GTPase to phagosomal surfaces, only the self-assembly mutation but

276 tates the maintenance of the RAB-7 GTPase on phagosomal surfaces.

277 es failure in recruiting the RAB-7 GTPase to phagosomal surfaces.

278 Phagosomal TLR responses in PI4KIIalpha-deficient DCs ar

279 hat PI4KIIalpha is an essential regulator of phagosomal TLR signaling in DCs by ensuring optimal TIRA

280 e and actin cytoskeleton and MyD88-dependent phagosomal TLR signaling, but not phagolysosome formatio

281 (PI4KIIalpha) plays a key role in initiating phagosomal TLR4 responses in murine DCs by generating a

282 The capacity to trigger phagosomal TLR9 recruitment was not affected by a loss o

283 Gram-negative bacteria by means of multiple phagosomal TLRs, resulting in de novo synthesis of Cxcl2

284 tracellular locations and is mediated by the phagosomal trafficking molecule adaptor protein-3 (AP-3)

285 Our studies further elucidate the effects of phagosomal trafficking on tailoring immune responses in

286 the NADPH oxidase complex, facilitating its phagosomal trafficking to induce a burst of reactive oxy

287 which M.tb inhibits both the activation and phagosomal translocation of SK1 to block the localized C

288 results suggest that preventing centripetal phagosomal transport delays the onset of acidification.

289 Suppression of the host phagosomal transport systems and the pathogen transporte

290 irst report of manipulation of intracellular phagosomal transport without interfering with the underl

291 ransporters, and the nine-member Francisella phagosomal transporter (Fpt) subfamily possesses homolog

292 The phagosomal transporter (Pht) family of the major facilit

293 roinflammatory cytokine secretion, abolishes phagosomal tubule formation, and impairs major histocomp

294 ligands and TLR stimulation, the late-onset phagosomal tubules are not essential for delivery of pha

295 Our data show that phagosomal tubules in DCs are functionally distinct from

296 oth LST-4 and SNX-1 promote the extension of phagosomal tubules to facilitate the docking and fusion

297 reveal that this IFN-beta induction requires phagosomal uptake and processing but bypasses the endoso

298 Therefore, avoidance of phagosomal uptake or subsequent escape from the phagosom

299 s with binding, uptake, and formation of the phagosomal vacuole, whereas recruitment of both TLR2 and

300 acid pH and reduced survival in an acidified phagosomal vacuole.