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 ation of promastigotes but not intracellular amastigotes.

5 (vii) promotion of survival of intracellular amastigotes.

6 y due to the difficulty in generating axenic amastigotes.

7 and contractile vacuole/spongiome complex of amastigotes.

8 ce IL-10 following infection with Leishmania amastigotes.

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

10 macrophages and transform into intracellular amastigotes.

11 ionary-phase promastigotes or tissue-derived amastigotes.

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

13 of gp91phox is recruited to PVs that harbor amastigotes.

14 ect vectors and fatty acids by intracellular amastigotes.

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

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

17 ented Pentostam sensitivity in intracellular amastigotes.

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

19 also forms surface-attached haptomonads and amastigotes.

20 e pathogenesis of intramacrophage Leishmania amastigotes.

21 not L. amazonensis infection established by amastigotes.

22 ncreasing DNA synthesis and proliferation of amastigotes.

23 racellular trypomastigotes and intracellular amastigotes.

24 ing the transformation of the parasites into amastigotes.

25 ia donovani and L. amazonensis intracellular amastigotes.

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

27 vely expressed in L. major promastigotes and amastigotes.

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

29 mspL and mspC class genes in tissue-derived amastigotes.

30 mastigotes became the most prominent form in amastigotes.

31 ion of avirulent promastigotes into virulent amastigotes.

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

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

34 ion of WT promastigotes into fully infective amastigotes.

35 electivity toward T. cruzi epimastigotes and amastigotes.

36 A promastigotes to differentiate into axenic amastigotes.

37 e green fluorescent protein reporter gene in amastigotes.

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

39 ch mRNA element is preferentially present in amastigotes.

40 a blood feed containing Leishmania mexicana amastigotes.

41 ive against replicative forms, in particular amastigotes.

42 nfective forms, metacyclic promastigotes and amastigotes.

43 the outer surface of the plasma membrane of amastigotes.

44 ivity than miltefosine against intracellular amastigotes.

45 inus and localizes to the plasma membrane of amastigotes.

46 TP synthesis than wild type in intracellular amastigotes.

47 ne localization in T. cruzi epimastigotes or amastigotes.

48 elated with promastigote transformation into amastigotes.

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

50 The axenic amastigotes also showed failure of basal body duplicatio

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

52 Amastigote and promastigote leishmania life stages retai

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

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 owed a progressive increase in the number of amastigotes and mononuclear inflammatory cells.

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

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

62 shmania, emphasizing the differences between amastigotes and promastigotes.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

77 Leishmania mexicana amastigotes are particularly rich in cysteine peptidases

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

79 equenced and found overexpressed in virulent amastigotes as compared with all other forms.

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

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

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

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

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

85 establishment of cellular immunity, and kill amastigotes but probably do not actively participate in

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

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

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

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

90 a from vaccinated mice to screen an L. major amastigote cDNA expression library.

91 r-infected BALB/c mice to screen an L. major amastigote cDNA expression library.

92 Sequence analysis of clones from an amastigote cDNA library confirmed the presence of gp63 m

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

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

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

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

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

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

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

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

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

106 the presence of Ca2+ signals in the virulent amastigotes during invasion of macrophages.

107 Amastigotes entered CHO cells by a cytochalasin D, genis

108 ed organellar acidification in permeabilized amastigotes, epimastigotes, and trypomastigotes of T. cr

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

110 In fact, axenic amastigotes expressing E152A LmAQP1 accumulated negligib

111 Leishmania promastigotes and amastigotes expressing LmAQP1 could regulate their volum

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

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

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

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

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

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

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

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 he effect of inhibitors on the intracellular amastigote form suggest that the life cycle is interrupt

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

123 g particularly numerous during metacyclic to amastigote form transformation.

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

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

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

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

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

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 However, upon conversion to amastigote forms within these host cells, the GPI-defici

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 ectively eliminated intracellular Leishmania amastigotes, further suggesting the importance of this p

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

164 vity when tested against Leishmania donovani amastigotes in vitro.

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

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

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

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

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

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

171 At a nonpermissive GPI deficiency, T. cruzi amastigotes inside mammalian cells replicated their sing

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

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

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

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

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

177 in L. mexicana amazonensis promastigotes and amastigotes is present in an acidic compartment rich in

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

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

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

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

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

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

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

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

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

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

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

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

190 2 mRNA levels in promastigotes compared with amastigotes must be controlled at the post-transcription

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

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

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

194 nes in promastigotes and axenically cultured amastigotes occurs at similar levels, as measured by nuc

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

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

197 Following s.c. inoculation with 5 x 10(6) amastigotes of L. mexicana into the shaven rump, STAT6+/

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

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

200 nfers Pentostam sensitivity in intracellular amastigotes of Leishmania.

201 Amastigotes of Trypanosoma cruzi express surface protein

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

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

204 r promastigote to the obligate intracellular amastigote parasite form.

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

206 Infections by amastigotes performed in the presence of metalloporphyri

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

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

209 Amastigotes present two classes of receptors for TGF-alp

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

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

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

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

214 ishmaniasis, the purified Leishmania pifanoi amastigote protein P-4 has been shown to induce signific

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

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

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

243 bility to differentiate to the intracellular amastigote stage.

244 Parasites transform intracellularly to the amastigote stage.

245 translation of subsets of transcripts in the amastigote stage.

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

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

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

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

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

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

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

253 ing the differentiation of trypomastigote to amastigote stages.

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

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

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

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

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

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

260 e Ca2+ is stored intracellularly in virulent amastigotes than in virulent promastigotes or avirulent

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

262 including IL-12 p70) by exposure to L. major amastigotes that ultimately accumulate in lesional tissu

263 ective to mammalian macrophages) rather than amastigotes (the form that parasitizes mammals); 2) they

264 ge of the parasite life cycle, compared with amastigotes, the intracellular stage of the life cycle t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

290 hmania mexicana amazonensis promastigotes or amastigotes were loaded with the fluorescent reagent fur

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

292 cellular L. chagasi amastigotes, whereas few amastigotes were present in the spleen.

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

294 ranulomas harboring intracellular L. chagasi amastigotes, whereas few amastigotes were present in the

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

296 Preferential opsonization of amastigotes with mannose-binding proteins may account fo

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

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

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

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