ライフサイエンスコーパス: amastigote

1 promastigote) to one with a 9+0 axoneme (the amastigote).

2 ocalized in the endoplasmic reticulum of the amastigote.

3 obust infection of the mammalian host by the amastigote.

4 e found to be lowest in actively replicating amastigotes.

5 nfective forms, metacyclic promastigotes and amastigotes.

6 the outer surface of the plasma membrane of amastigotes.

7 inus and localizes to the plasma membrane of amastigotes.

8 TP synthesis than wild type in intracellular amastigotes.

9 ne localization in T. cruzi epimastigotes or amastigotes.

10 elated with promastigote transformation into amastigotes.

11 (vii) promotion of survival of intracellular amastigotes.

12 y due to the difficulty in generating axenic amastigotes.

13 and contractile vacuole/spongiome complex of amastigotes.

14 ce IL-10 following infection with Leishmania amastigotes.

15 in IL-10 production induced by IgG-opsonized amastigotes.

16 ionary-phase promastigotes or tissue-derived amastigotes.

17 ion in yeast and in L. amazonensis LIT1-null amastigotes.

18 of gp91phox is recruited to PVs that harbor amastigotes.

19 ect vectors and fatty acids by intracellular amastigotes.

20 s enzyme subunit is found in PVs that harbor amastigotes.

21 x, in contrast to only 2% of PVs that harbor amastigotes.

22 ented Pentostam sensitivity in intracellular amastigotes.

23 host cells and replicate intracellularly as amastigotes.

24 lpg2(-)REV amastigotes resemble L. mexicana amastigotes.

25 e pathogenesis of intramacrophage Leishmania amastigotes.

26 not L. amazonensis infection established by amastigotes.

27 ncreasing DNA synthesis and proliferation of amastigotes.

28 racellular trypomastigotes and intracellular amastigotes.

29 ing the transformation of the parasites into amastigotes.

30 ation of promastigotes but not intracellular amastigotes.

31 also forms surface-attached haptomonads and amastigotes.

32 A promastigotes to differentiate into axenic amastigotes.

33 ivity than miltefosine against intracellular amastigotes.

34 macrophages and transform into intracellular amastigotes.

35 ia donovani and L. amazonensis intracellular amastigotes.

36 y is suggested for the entry of aspartate in amastigotes.

37 PPDK is involved in the entry of alanine in amastigotes.

38 ion of avirulent promastigotes into virulent amastigotes.

39 es as well as L. amazonensis and L. infantum amastigotes.

40 wild-type (WT) promastigotes into infective amastigotes.

41 ion of WT promastigotes into fully infective amastigotes.

42 electivity toward T. cruzi epimastigotes and amastigotes.

43 e green fluorescent protein reporter gene in amastigotes.

44 stigotes, and the Fc receptor (FcR), used by amastigotes.

45 ch mRNA element is preferentially present in amastigotes.

46 a blood feed containing Leishmania mexicana amastigotes.

47 ive against replicative forms, in particular amastigotes.

48 We show that surface IgG on Leishmania amastigotes allows them to ligate Fc gamma receptors on

49 The axenic amastigotes also showed failure of basal body duplicatio

50 in the differentiation of trypomastigotes to amastigotes, an essential step for the intracellular rep

51 Amastigote and promastigote leishmania life stages retai

52 C, inhibited growth of wild-type L. donovani amastigotes and effectively cured macrophages of parasit

53 ty against Leishmania donovani intracellular amastigotes and excellent selectivity (>660-fold) for Le

54 the infective parasite stages (intracellular amastigotes and extracellular trypomastigotes).

55 growth of both L. donovani promastigotes and amastigotes and intimate that pharmacological inhibition

56 eogenesis is an active pathway in Leishmania amastigotes and is essential for their survival within t

57 Ldp27) that was more abundantly expressed in amastigotes and metacyclic promastigotes than in procycl

58 Our results demonstrate that amastigotes and metacyclics efficiently enter and activa

59 rly expression of TcPI-PLC on the surface of amastigotes and PIP(2) depletion coincide with host cyto

60 the proliferation of intracellular T. cruzi amastigotes and produced a profound suppression in the n

61 shmania, emphasizing the differences between amastigotes and promastigotes.

62 n specifically in infectious metacyclics and amastigotes and promoting parasite survival in the host.

63 hat TcPI-PLC is developmentally regulated in amastigotes and shows two peaks of surface expression du

64 xtracellular phase of the plasma membrane of amastigotes and that its N-terminal 20 amino acids are n

65 calizes to the surface of Leishmania pifanoi amastigotes and that upon exposure to macrophages, P8 PG

66 fter differentiation of trypomastigotes into amastigotes and the second before differentiation of ama

67 plasmic reticulum location was also found in amastigotes and trypomastigotes using a polyclonal antib

68 malian intracellular replicating life stage (amastigote), and uncover implications of starvation-indu

69 ivatives showed high activity against axenic amastigotes, and among them, compound 5g (4-(((3,4,5-tri

70 ar localization of LmPRL-1 in promastigotes, amastigotes, and infected macrophages, we found that the

71 wth of Leishmania donovani promastigotes and amastigotes, and iron did not play a significant role in

72 o invade mammalian hosts, differentiate into amastigotes, and replicate inside macrophages.

73 form, promastigotes, to the vertebrate form, amastigotes, and survival inside the vertebrate host acc

74 ons of DC signaling pathways and function by amastigotes, and the impact of DC functions on protectiv

75 aled that TcGP63 is 61 kDa in epimastigotes, amastigotes, and tissue culture-derived trypomastigotes

76 The Leishmania pifanoi amastigote antigen P-8 has been previously shown to indu

77 ith the developmentally regulated Leishmania amastigote antigen, P-8.

78 However, ACs in spt2- amastigotes appeared quantitatively and morphologically

79 Leishmania mexicana amastigotes are particularly rich in cysteine peptidases

80 Similarly, amastigotes are re-sensitized to azoles following additi

81 ation; however, the intracellular parasites (amastigotes) are capable of down-modulating LPS/IFN-gamm

82 tion both to metacyclic promastigotes and to amastigotes, autophagosomes being particularly numerous

83 to gain insight into the mechanism by which amastigotes avoid eliciting superoxide production.

84 Taken together, we propose that Leishmania amastigotes avoid superoxide production by inducing an i

85 the production of superoxide, infections by amastigotes barely induce superoxide production.

86 -)) showed selective growth arrest as axenic amastigotes but not as promastigotes.

87 cytokinesis and viability of disease-causing amastigotes but not for flagellar membrane trafficking.

88 We confirmed that L. major amastigotes, but not promastigotes, efficiently entered

89 ferentiation of metacyclic promastigotes and amastigotes, but the parasites failed to replicate after

90 ferent receptors detecting promastigotes and amastigotes, but the relative importance of each interac

91 e is partially due to the IL-4 production by amastigote-carrying DCs.

92 LB/c mice to screen a Leishmania amazonensis amastigote cDNA expression library and obtained the full

93 identifying cDNA sequences in an L. donovani amastigote cDNA library that collectively or singly conf

94 icant increase in MIL-R in the intracellular amastigote compared to the corresponding wild-type did n

95 tivity was observed in centrin mutant axenic amastigotes compared with wild type cells, suggesting th

96 51 and significant activity against T. cruzi amastigotes cultured in human myoblasts (EC50 = 14-18 nM

97 It selectively induced amastigote death at doses similar to amphotericin B dose

98 ial role for LIT1 in intracellular growth as amastigotes, Deltalit1 parasites were avirulent.

99 studies employing tissue-derived (opsonized) amastigotes demonstrated that L. pifanoi-infected FcR(-/

100 s display defective intracellular killing of amastigotes despite normal expression of TNF and NO synt

101 y released/secreted by both promastigote and amastigote developmental forms of this parasite.

102 ccumulated superoxide radicals and initiated amastigote differentiation after exposure to H(2)O(2) bu

103 polyPs was detected during trypomastigote to amastigote differentiation and during the lag phase of g

104 y by the parasite to undergo promastigote to amastigote differentiation in vitro.

105 However, the signaling events controlling amastigote differentiation remain poorly understood.

106 able as insect form promastigotes but not as amastigotes, do not take up glucose and other hexoses bu

107 Amastigotes entered CHO cells by a cytochalasin D, genis

108 Upon transfer into syngeneic recipients, amastigote-exposed BALB/c DCs prime parasite-specific Th

109 In fact, axenic amastigotes expressing E152A LmAQP1 accumulated negligib

110 Leishmania promastigotes and amastigotes expressing LmAQP1 could regulate their volum

111 Infection with amastigotes fails to induce CD40-dependent IL-12 product

112 long been appreciated, the importance of the amastigote flagellum has often been disregarded.

113 We propose that the main function of the amastigote flagellum is to act as a sensory organelle wi

114 recent work suggests that the 'rudimentary' amastigote flagellum may serve indispensable roles in ce

115 erated a cDNA library from the intracellular amastigote form of Leishmania chagasi, the cause of Sout

116 versus the clinically relevant intracellular amastigote form of T. cruzi, but only a approximately 1-

117 However, whether the infectious or amastigote form of the parasite requires an intact polya

118 s of this method against the differentiated, amastigote form of the parasite using three distinct via

119 indicating active pyrimidine salvage by the amastigote form of the parasite, but the Deltacps/Deltau

120 tly expressed on the intracellular mammalian amastigote form of the protozoan parasite, and tuzin is

121 infective stage of the parasite, but not the amastigote form that exists in the mammalian host.

122 g particularly numerous during metacyclic to amastigote form transformation.

123 mol/mg of protein, respectively, and for the amastigote form, the corresponding concentrations were 3

124 ed the parasite in the macrophage-associated amastigote form.

125 n in vitro studies against the intracellular amastigotes form of Leishmania donovani.

126 ently block the growth of the intracellular (amastigote) form of T. cruzi grown in fibroblast host ce

127 rulence factor for survival of intracellular amastigote forms in the mammalian host.

128 ssful cytokinesis and survival of infectious amastigote forms inside mammalian macrophages.

129 8% inhibition of growth of the intracellular amastigote forms of L. donovani and T. cruzi, respective

130 This study showed that both promastigote and amastigote forms of Sb(R)LD, but not the antimony-sensit

131 Exposure of trypomastigote and amastigote forms of T. cruzi to defensin alpha-1 signifi

132 Both promastigote and amastigote forms of the parasite were found.

133 parasites alternate between promastigote and amastigote forms which differ significantly in cellular

134 gene replacement, is unable to replicate as amastigote forms within phagolysomes of mammalian host m

135 ogenous glutamine protects actively dividing amastigotes from ergosterol biosynthesis inhibitors (azo

136 anuloma formation and effective clearance of amastigotes from foci of infection in the hepatic parenc

137 t host cell signaling and to form infectious amastigotes from the few parasites surviving the establi

138 a 31-kDa cysteine proteinase associated with amastigote glycolipids.

139 The centrin null mutant defective in amastigote growth could be useful as a vaccine candidate

140 d in the absence of such synergy it promotes amastigote growth.

141 -/-) parasites confirmed the role of Ufm1 in amastigote growth.

142 ry analysis confirmed that the mutant axenic amastigotes have a cell cycle arrest at the G(2)/M stage

143 nd 5.42 muM, respectively) and intracellular amastigote (IC(50) 9.81 and 3.75 muM, respectively) form

144 vity against Trypanosoma cruzi intracellular amastigotes (IC(50) ranging from 28 nM to 3.72 muM) with

145 bition on the proliferation of intracellular amastigotes (IC(70) = 29 nM), while complex 8 displayed

146 eishmanicidal activity against intracellular amastigotes (IC50 from 0.65 +/- 0.2 to 7.76 +/- 2.1 muM)

147 gammaRIII on some other cell engaged by IgG1-amastigote immune complexes induces IL-10 from T cells.

148 y, possible roles of the P-4 nuclease in the amastigote in RNA stability (gene expression) or DNA rep

149 n life cycle morphologies: the intracellular amastigote in the mammalian host and the promastigote in

150 g the differentiation of virulent Leishmania amastigotes in a process regulated by iron availability.

151 nzyme trypanothione reductase of replicating amastigotes in hosts' reticuloendothelial tissues.

152 The defect in vitro growth of amastigotes in human macrophages was further substantiat

153 ificantly enhanced the growth of L. donovani amastigotes in human macrophages.

154 ith the different fates of promastigotes and amastigotes in IFN-gamma-stimulated Mphis, L. amazonensi

155 the intracellular proliferation of T. cruzi amastigotes in infected macrophages in a concentration-d

156 Growth of LdCEN(-/-) amastigotes in infected macrophages in vitro was inhibit

157 m disappearance of lesions; disappearance of amastigotes in lesion sites, as determined by histopatho

158 esistant promastigotes when transformed into amastigotes in macrophage cells cannot be cured by treat

159 omastigotes in sand flies and nonflagellated amastigotes in mammals, causing a spectrum of serious di

160 ed that the growth of Leishmania amazonensis amastigotes in murine macrophages (Mphis) was enhanced i

161 that ROS inhibits growth of L. braziliensis amastigotes in resting monocytes, and that classical mon

162 he gut lumen of their sandfly vectors and as amastigotes in the phagolysosomal compartments of infect

163 acellular growth, since the concentration of amastigotes in the site was not enhanced compared to tha

164 was associated with an increasing number of amastigotes in the site, the low-dose model revealed a r

165 mpounds display potency for killing T. cruzi amastigotes in vitro with values of EC(50) in the 0.4-10

166 vity when tested against Leishmania donovani amastigotes in vitro.

167 cted in replicative stages (epimastigote and amastigote), in which heme transport activity was previo

168 he differentiation of Leishmania amazonensis amastigotes, independently of temperature and pH changes

169 n vitro experiments indicate that L. pifanoi amastigotes induce lower levels of cytokines in macropha

170 subcellular fractions enriched with PVs from amastigote-infected cells and probed with antibodies to

171 yers with either rIL-10 or supernatants from amastigote-infected macrophages resulted in a dramatic e

172 in-12p40 production following L. amazonensis amastigote infection compared with non-treated, infected

173 Notably, L. amazonensis amastigote infection failed to activate DCs, and this la

174 most phagocytic processes described to date, amastigote internalization in CHO cells involved activat

175 tes and the second before differentiation of amastigotes into trypomastigotes.

176 that TLR4 recognition of Leishmania pifanoi amastigotes is important for the control of infection an

177 nsect promastigotes into mammalian-infective amastigotes is induced by elevated temperature and low p

178 FN degradation at the surfaces of amastigotes is leishmanolysin dependent, whereas both se

179 vertant-infected mice exhibited lesions, and amastigotes isolated from these lesions were able to rep

180 owever, LFR1 overexpression is not toxic for amastigotes lacking the ferrous iron transporter LIT1 an

181 n of macrophages with Leishmania amazonensis amastigotes led to the activation of the MAPK, ERK1/2.

182 and in vitro activity against T. brucei and amastigote Leishmania infantum.

183 ctor (i.e. promastigote) and mammalian (i.e. amastigote) life cycle developmental forms of this proto

184 t these parasites converted to extracellular amastigote-like cells and metacyclic trypomastigotes mor

185 M against cultured T. brucei and L. donovani amastigote-like forms, surpassing the activity of compou

186 as supported by the fact that L. amazonensis amastigotes limited the production of IL-12p40 from BM-D

187 Mass spectrometry of spt2- amastigote lipids revealed the presence of high levels o

188 subunit IV at mammalian temperature, and in amastigotes, LmCOX activity and mitochondrial function w

189 dily secrete IL-10 in response to IgG-coated amastigotes, making macrophages a prime candidate as the

190 These results suggest that L. amazonensis amastigotes may condition DCs of a susceptible host to a

191 nse observed, indicating that the intact P-4 amastigote molecule, rather than selected peptides, may

192 Changes in amastigote morphology and ultrastructure were assessed b

193 ctive proinflammatory response and inhibited amastigote multiplication in infected J774 macrophages a

194 a on the EVs produced by trypomastigotes and amastigotes (N.

195 ogy showed fibrinoid vascular necrosis, rare amastigote nests within skeletal muscle myocytes, and ma

196 sented with inflammatory foci, necrosis, and amastigote nests.

197 ctive with IC(50) values against L. donovani amastigotes of 0.5 +/- 0.2 and 2.3 +/- 0.8 microM, respe

198 this study, we successfully generated axenic amastigotes of L. braziliensis and used them to test the

199 tha, and their effects against intracellular amastigotes of Leishmania (L.) infantum evaluated in vit

200 indings and show that both promastigotes and amastigotes of Leishmania species can bind directly to s

201 These studies indicate that amastigotes of Leishmania use an unusual and unexpected

202 nfers Pentostam sensitivity in intracellular amastigotes of Leishmania.

203 Amastigotes of Trypanosoma cruzi express surface protein

204 n developmental forms (i.e. promastigote and amastigotes) of this organism.

205 tion of inflammatory macrophages (Mphi) with amastigotes or promastigotes did not lead to significant

206 n the entry of glycerol in promastigotes and amastigotes; PEPCK participates in the entry of aspartat

207 Infections by amastigotes performed in the presence of metalloporphyri

208 of SLs and other molecules by intracellular amastigotes play key roles in AC biogenesis and parasite

209 Here we show that Trypanosoma cruzi amastigotes possess a higher Ca2+ content than the extra

210 Amastigotes present two classes of receptors for TGF-alp

211 ubilized trypomastigotes, epimastigotes, and amastigotes probed with anti-recombinant Tc-1 immunoglob

212 f macrophages to TGF-alpha induced increased amastigote proliferation.

213 n of FcgammaRs with IgG-opsonized Leishmania amastigotes promotes IL-10 production by macrophages.

214 ified membrane-associated Leishmania pifanoi amastigote protein P-4 has been shown to induce protecti

215 se data support a model in which L. donovani amastigotes readily salvage ornithine and have some acce

216 Amastigotes recovered from these lesions were fully infe

217 Endogenous LIT1 was only detectable in amastigotes replicating intracellularly, and its intrace

218 LdCen1(-/-) has a defect in amastigote replication both in vitro and ex vivo in huma

219 that IFN-gamma could promote L. amazonensis amastigote replication in macrophages (Mphis), although

220 Persisting amastigote replication in the S. mansoni egg granulomas

221 nd, IFN-gamma could stimulate Mphis to limit amastigote replication when it was coupled with lipopoly

222 Thus, in some respects, the lpg2(-)REV amastigotes resemble L. mexicana amastigotes.

223 Amastigote resistance is concomitant with the overexpres

224 l clones generated against Leishmania: major amastigotes responded to Leishmania:-infected macrophage

225 y when strains were assayed as intracellular amastigotes: responsive isolates ED50=2.4+/-2.6, ED90=6.

226 f the centrin genes (centrin1) in Leishmania amastigotes resulted in failure of both basal body dupli

227 -derived dendritic cells with L. amazonensis amastigotes resulted in rapid and significant phosphoryl

228 Electron microscopy of SUB knock-out amastigotes revealed abnormal membrane structures, retai

229 ctural investigations of Leishmania mexicana amastigotes revealed structures that were tentatively id

230 Firstly, axenic amastigotes showed higher infectivity and the potential

231 Although gcvP(-) promastigotes and amastigotes showed normal virulence in macrophage infect

232 However, lpg2(-) L. mexicana amastigotes similarly lacking PGs but otherwise normal i

233 -8 epitope is associated with the L. pifanoi amastigote-specific glycolipid components found in the t

234 ein E (derived from fetal bovine serum), and amastigote-specific glycolipids.

235 normally into aflagellated forms expressing amastigote-specific markers but were not able to replica

236 Previously, we had shown that the amastigote-specific protein p27 (Ldp27) is a component o

237 s selectively expressed in the intracellular amastigote stage (mammalian host) but not in the promast

238 immunoglobulin G-mediated mechanisms for the amastigote stage in the host is evident; however, the im

239 (-/-) mutants showed reduced survival in the amastigote stage in vitro and ex vivo in human macrophag

240 and selective in vitro activity against the amastigote stage of L. infantum while no activity was ob

241 of these null mutants in the disease-causing amastigote stage of the life cycle.

242 NT4 is required for optimal viability of the amastigote stage of the parasite that lives within acidi

243 tant for mRNA abundance in the intracellular amastigote stage of the parasite.

244 y toxic toward T. cruzi in the intracellular amastigote stage.

245 bility to differentiate to the intracellular amastigote stage.

246 Parasites transform intracellularly to the amastigote stage.

247 translation of subsets of transcripts in the amastigote stage.

248 oduct of the beta-oxidation in the Ufm1(-/-) amastigote stage.

249 osoma brucei and probably the intracellular (amastigote) stage of Trypanosoma cruzi derive all of the

250 The intracellular amastigote stages of parasites such as Leishmania are of

251 as surface proteins in trypomastigote and/or amastigote stages of T. cruzi.

252 s been detected in both the promastigote and amastigote stages of the Leishmania life cycle.

253 essed at high levels in the epimastigote and amastigote stages of the parasite, and its expression is

254 forms (the insect epimastigote and mammalian amastigote stages) and the non-dividing trypomastigote s

255 ing the differentiation of trypomastigote to amastigote stages.

256 that carbons from (13)C-glutamine feed into amastigote sterols and into metabolic intermediates that

257 8 in infected humans, hamsters, and parasite amastigotes suggested its importance for disease persist

258 ypomastigote surface antigen, TSA-1, and two amastigote surface molecules, ASP-1 and ASP-2, were rece

259 epitopes in two recently described T. cruzi amastigote surface proteins, ASP-1 and ASP-2.

260 urrent proposals that GIPLs are required for amastigote survival in the mammalian host or that parasi

261 protein or protein complex more abundant in amastigotes than in epimastigotes binds to this minimall

262 n mRNA, however, is 68-fold more abundant in amastigotes than in epimastigotes.

263 lf-life of amastin mRNA is 7 times longer in amastigotes than in epimastigotes.

264 We describe a gene first identified in amastigotes that is essential for survival inside the ho

265 In the pathogenic amastigote, the mammalian stage of Leishmania parasites,

266 Upon binding of TGF-alpha to amastigotes, the ligand is internalized, inducing trypan

267 take in orchestrating the differentiation of amastigotes, through a mechanism that involves productio

268 L. amazonensis amastigotes, through activation of extracellular signal-

269 vents metacyclogenesis and transformation to amastigotes, thus adding support to the hypothesis that

270 of host glutamine metabolism that sensitizes amastigotes to azoles.

271 This IgG allows amastigotes to exploit the antiinflammatory effects of F

272 y interactions as the parasites develop from amastigotes to infectious metacyclics, highlighting rece

273 from the parasitophorous vacuole to liberate amastigotes to multiply freely in the cytosol.

274 e results describe a novel mechanism used by amastigotes to regulate their proliferation mediated by

275 Deltaodc lesion also affected the ability of amastigotes to sustain a robust infection, macrophage an

276 precursor in mammals, was used by Leishmania amastigotes to synthesize mannogen, entering the pathway

277 LmGT2 RNA decay in promastigotes and axenic amastigotes treated with actinomycin D suggests that dif

278 deficient Ms are defective in IgG1-opsonized amastigote uptake.

279 icana CPA/CPB-deficient mutants transform to amastigotes very poorly and lack virulence in macrophage

280 es demonstrated that the compound eliminates amastigotes via an independent activation of the host ce

281 Mutant parasites demonstrated diminished amastigote viability and delayed lesion development in m

282 t metabolite is responsible for the L. major amastigote virulence defect, although further studies ru

283 he role of glycoconjugates other than PGs in amastigote virulence, while providing further support fo

284 e replication of single copy lack mutants as amastigotes was attenuated in macrophages in vitro, and

285 , the intracellular growth of LHR1/Deltalhr1 amastigotes was fully restored when macrophages were all

286 replication-promoting effect of IFN-gamma on amastigotes was independent of the source and genetic ba

287 trated that IgG on the surface of Leishmania amastigotes was required to achieve maximal IL-10 produc

288 ntly not affected by surface opsonization of amastigotes, was not mediated by interleukin-10 or trans

289 ic entry in the intracellular persistence of amastigotes, we examined the invasion of Chinese hamster

290 ODC-deficient promastigotes and axenic amastigotes were auxotrophic for polyamines and capable

291 Interestingly, however, amastigotes were found to secrete/release approximately

292 y progressive lesions appeared, and purified amastigotes were fully virulent to macrophages and mice.

293 n uptake was mediated by fibronectin or when amastigotes were opsonized with immunoglobulin G and int

294 the differentiation of trypomastigotes into amastigotes, where TcPI-PLC associates with the plasma m

295 espective of infection with promastigotes or amastigotes, whereas this was the case only when promast

296 lagellated trypomastigotes remodel into oval amastigotes with no external flagellum.

297 mately 3.1-kb mRNA in both promastigotes and amastigotes, with homologues being detected in several o

298 s an effective method to kill host-infective amastigotes, with morphological changes consistent with

299 tants are strongly compromised for growth as amastigotes within host macrophages.

300 ufficient to activate macrophages to destroy amastigotes within parasitized lesions.