ライフサイエンスコーパス: F. tularensis

1 F. tularensis activates complement, and recent data sugg

2 F. tularensis also significantly impaired apoptosis trig

3 F. tularensis can also invade and replicate in a variety

4 F. tularensis DNA in buffer or CFU of F. tularensis was

5 F. tularensis has long been developed as a biological we

6 F. tularensis infects leukocytes and exhibits an extrace

7 F. tularensis LVS::Deltawzy expressed only 1 repeating u

8 F. tularensis represses inflammasome; a cytosolic multi-

9 F. tularensis subspecies encode a series of acid phospha

10 F. tularensis subspecies holarctica was isolated from th

11 F. tularensis virulence stems from genes encoded on the

12 eriments in F. tularensis identified over 50 F. tularensis DsbA substrates, including outer membrane

13 d protective effects against virulent type A F. tularensis challenge.

14 ainst aerosol challenge with virulent type A F. tularensis in a species other than a rodent since the

15 7 is dispensable for host immunity to type A F. tularensis infection, and that induced and protective

16 during intracellular infections with type A F. tularensis.

17 Infection of mice in vivo with a F. tularensis LVS FTL_0724 mutant resulted in diminished

18 In contrast, infection of macrophages with a F. tularensis LVS rluD pseudouridine synthase (FTL_0699)

19 t against intentional release of aerosolized F. tularensis, the most dangerous type of exposure.

20 cyte-derived DCs (Mo-DCs) in the lungs after F. tularensis LVS pulmonary infection.

21 roader spectrum of growth inhibition against F. tularensis , Bacillus anthracis , and Staphylococcus

22 y potential correlates of protection against F. tularensis and to expand and refine a comprehensive s

23 ific immune responses and protection against F. tularensis challenge.

24 nous interleukin 12 (IL-12) protects against F. tularensis infection; this protection was lost in MII

25 ous vaccine-induced immune responses against F. tularensis.

26 Although F. tularensis is a recognized biothreat agent with broad

27 ltiple differences between species and among F. tularensis subspecies and subpopulations.

28 inase activities were observed to vary among F. tularensis and F. novicida strains.

29 An F. tularensis subsp. tularensis trpB mutant is also atte

30 ogenesis and define FTL_0883/FTT_0615c as an F. tularensis gene important for virulence and evasion o

31 strains induced low levels of cytokines, an F. tularensis ripA deletion mutant (LVSDeltaripA) provok

32 Consistent with this function, an F. tularensis subsp. novicida trpB mutant is unable to g

33 Using an F. tularensis Schu S4 mutant library, we identified stra

34 F. tularensis subsp. tularensis (type A) and F. tularensis subsp. holarctica (type B).

35 hown to modulate both isomerase activity and F. tularensis virulence.

36 polar bears to C. burnetii, N. caninum, and F. tularensis.

37 othenate pathway in Francisella novicida and F. tularensis and identified an unknown and previously u

38 s in human virulence between F. novicida and F. tularensis may be due in part to the absence of cdGMP

39 ture supernatant in vitro by F. novicida and F. tularensis subsp. holarctica LVS.

40 F. novicida and F. tularensis subspecies failed to stimulate reactive ox

41 Such outbreaks are exceedingly rare, and F. tularensis is seldom recovered from clinical specimen

42 nd to differ between Francisella species and F. tularensis subspecies and subpopulations.

43 tial for misidentification of F. novicida as F. tularensis.

44 en identified 95 lung infectivity-associated F. tularensis genes, including those encoding the Lon an

45 rotective immune response against attenuated F. tularensis versus F. tularensis type A differs.

46 tion of antibodies from patients with type B F. tularensis infections and that these can be used for

47 tification and differentiation of tick-borne F. tularensis.

48 eration of AA to be converted into PGE(2) by F. tularensis-infected macrophages.

49 ecessary for classical pathway activation by F. tularensis in nonimmune human serum nor the receptors

50 tion, and suppression of their activation by F. tularensis is likely a mechanism that aids in bacteri

51 veals novel pathogenic mechanisms adopted by F. tularensis to modulate macrophage innate immune funct

52 tularensis vs Pseudomonas aeruginosa and by F. tularensis live bacteria vs the closely related bacte

53 e previous reports, induction of IFN-beta by F. tularensis was not required for activation of the inf

54 hat metabolic reprogramming of host cells by F. tularensis is a key component of both inhibition of h

55 ector memory (EM) CD4(+) T cells elicited by F. tularensis infection (postimmunization) is increased

56 e FabI enoyl-ACP-reductase enzyme encoded by F. tularensis is essential and not bypassed by exogenous

57 mechanisms of host innate immune evasion by F. tularensis.

58 e for this suppression of innate immunity by F. tularensis are not defined.

59 ation of host cell death during infection by F. tularensis and highlight how shifts in the magnitude

60 he establishment of a fulminate infection by F. tularensis.

61 unidentified mechanism for uptake of iron by F. tularensis.

62 the mechanisms of inflammasome repression by F. tularensis.

63 iously demonstrated that PGE(2) synthesis by F. tularensis-infected macrophages requires cytosolic ph

64 infected antigen presenting cells to control F. tularensis LVS intracellular growth.

65 (live vaccine strain) or catalase-deficient F. tularensis (DeltakatG) show distinct profiles in thei

66 new cartridge-based assay can rapidly detect F. tularensis in bloodstream infections directly in whol

67 In infected macaques, the assay detected F. tularensis on days 1 to 4 postinfection in 21%, 17%,

68 tection against challenge with two different F. tularensis subsp. holarctica (type B) live vaccine st

69 . coli cells yielded glycOMVs that displayed F. tularensis O-PS.

70 erosolizable nature and low infectious dose, F. tularensis is classified as a category A select agent

71 During F. tularensis subspecies novicida infection, AIM2, an in

72 ly with the extent of necrotic damage during F. tularensis infection.

73 eveal a novel intraerythrocytic phase during F. tularensis infection.

74 .n., with MAb-iFT immune complexes, enhances F. tularensis-specific immune responses and protection a

75 To establish F. tularensis FabI (FtFabI) as a clinically relevant dru

76 y, human neutrophil uptake of GFP-expressing F. tularensis strains live vaccine strain and Schu S4 wa

77 nes, immunotherapeutics, and diagnostics for F. tularensis requires a detailed knowledge of the sacch

78 ted first that C1q and C3 were essential for F. tularensis phagocytosis, whereas C5 was not.

79 nicity island genes tested are essential for F. tularensis Schu S4 virulence and further suggest that

80 igase gene (FTL_0724) as being important for F. tularensis live vaccine strain (LVS) virulence.

81 kinase 3 (JAK3) signaling are necessary for F. tularensis-induced PGE2 production.

82 The activity observed for F. tularensis strains was predominantly associated with

83 ent delay in host cell death is required for F. tularensis to preserve its intracellular replicative

84 aled that lon and clpP are also required for F. tularensis tolerance to stressful conditions.

85 TL_1548 and FTL_1709, which are required for F. tularensis virulence.

86 Moreover, p38 MAPK activity is required for F. tularensis-induced COX-2 protein synthesis, but not f

87 to inhibit the activity of purified DXR from F. tularensis LVS (IC(50)=230 nM).

88 in inhibits purified MEP synthase (DXR) from F. tularensis LVS.

89 vel bacterial carboxylesterase (FTT258) from F. tularensis, a homologue of human acyl protein thioest

90 signal transducer and model drug by LPS from F. tularensis vs Pseudomonas aeruginosa and by F. tulare

91 and subsp. holarctica (type B) strains from F. tularensis subsp. novicida and other near neighbors,

92 Furthermore, F. tularensis LVS delayed pyroptotic cell death of the i

93 Since current methods used to genotype F. tularensis are time-consuming and require extensive l

94 Several in vivo screens have identified F. tularensis genes necessary for virulence.

95 Our objective was to identify F. tularensis-activated host signaling pathways that reg

96 atty acid biosynthetic components encoded in F. tularensis are transcriptionally active during infect

97 nal role of OxyR has not been established in F. tularensis.

98 tern of endogenous protein-tagging events in F. tularensis that are likely to be a universal feature

99 Trapping experiments in F. tularensis identified over 50 F. tularensis DsbA subs

100 described as virulence-associated factors in F. tularensis Identification of these Lon substrates has

101 and FTT_0615c, the homologue of FTL_0883 in F. tularensis subsp. tularensis Schu S4 (Schu S4), elici

102 However, in F. tularensis-infected macrophages we observed a tempora

103 ication of genes encoding a Kdo hydrolase in F. tularensis Schu S4 and live vaccine strain strains, i

104 the evaluation of chiA and chiC knockouts in F. tularensis A1 and A2 strains, respectively, provided

105 is also required for lipid A modification in F. tularensis as well as Bordetella bronchiseptica.

106 Analysis of the MglA and SspA mutants in F. tularensis reveals that interaction between PigR and

107 Only the OxyR homolog is present in F. tularensis, while the SoxR homologs are absent.

108 S transporters may play an important role in F. tularensis pathogenesis and serve as good targets for

109 in part to the absence of cdGMP signaling in F. tularensis.

110 amework for understanding the role of T4P in F. tularensis virulence.

111 potential therapeutic agent against inhaled F. tularensis that prolongs survival and the opportunity

112 susceptible than IgA(+/+) mice to intranasal F. tularensis LVS infection, despite developing higher l

113 ase, implicate the enzyme as a potential key F. tularensis effector protein, and may help elucidate a

114 pressed secretion in response to heat-killed F. tularensis.

115 membrane protein 2 localization with labeled F. tularensis in the lungs was greater in wild-type than

116 s involved in bacterial immune evasion, like F. tularensis clpB, can serve as a model for the rationa

117 Living F. tularensis live vaccine strain and Schu S4 did not st

118 equivalents (GE) per reaction and 10 CFU/ml F. tularensis in both human and macaque blood.

119 nged the survival of treated mice after i.n. F. tularensis challenge relative to mock treated animals

120 Collectively, this study reports a novel F. tularensis factor that is required for innate immune

121 pic differences by evaluating the ability of F. tularensis and F. novicida to degrade chitin analogs

122 The ability of F. tularensis subsp. novicida to recapitulate the key ph

123 echanism of immune evasion is the ability of F. tularensis to induce the synthesis of the small lipid

124 efense mechanisms, as well as the ability of F. tularensis to prolong neutrophil lifespan.

125 Based on the ability of F. tularensis to resist high ROS/RNS levels, we have hyp

126 Multiple independent acquisitions of F. tularensis from the environment over a short time per

127 wever, the factors that govern adaptation of F. tularensis to the intrahepatocytic niche have not bee

128 del wherein the immunomodulatory capacity of F. tularensis relies, at least in part, on TolC-secreted

129 F. tularensis DNA in buffer or CFU of F. tularensis was spiked into human or macaque blood.

130 The outbreak was caused by diverse clones of F. tularensis that occurred concomitantly, were widespre

131 ypothesized that the antioxidant defenses of F. tularensis maintain redox homeostasis in infected mac

132 We demonstrate that antioxidant enzymes of F. tularensis prevent the activation of redox-sensitive

133 Escape of F. tularensis from the phagosome into the cytosol of the

134 One significant virulence factor of F. tularensis is the O-polysaccharide (O-PS) portion of

135 n for alternative proinflammatory factors of F. tularensis LVS identified the heat shock protein GroE

136 ur results also demonstrate that FTL_0325 of F. tularensis impacts proIL-1beta expression as early as

137 ) form of the enzyme and inhibited growth of F. tularensis SchuS4 at concentrations near that of thei

138 A hallmark of F. tularensis virulence is its ability to quickly grow t

139 reased cell death with a 2-3 log increase of F. tularensis replication, but could be rescued with rIL

140 uding spermine, regulate the interactions of F. tularensis with host cells.

141 screening a transposon insertion library of F. tularensis LVS in the presence of hydrogen peroxide,

142 re region of the lipopolysaccharide (LPS) of F. tularensis to probe antigenic responses elicited by a

143 profile of the live vaccine strain (LVS) of F. tularensis grown in the FL83B murine hepatocytic cell

144 nfection by the live vaccine strain (LVS) of F. tularensis Resistance is characterized by reduced let

145 f mice with the live vaccine strain (LVS) of F. tularensis, splenic IL-10 levels increased rapidly an

146 cells with the live vaccine strain (LVS) of F. tularensis.

147 oterrorism, but the pathogenic mechanisms of F. tularensis are largely unknown.

148 ovide fundamental insight into mechanisms of F. tularensis phagocytosis and support a model whereby n

149 revealed novel immune evasive mechanisms of F. tularensis.

150 ty and the antioxidant defence mechanisms of F. tularensis.

151 ished Kdo hydrolase activity in membranes of F. tularensis live vaccine strain.

152 Through transposon mutagenesis of F. tularensis subsp. holarctica live vaccine strain (LVS

153 Utilizing a mutant of F. tularensis in FTL_0325 gene, this study investigated

154 Significantly, trans-translation mutants of F. tularensis are impaired in replication within macroph

155 ignment of the inner core oligosaccharide of F. tularensis .

156 ays an important role in the pathogenesis of F. tularensis and suggest that a focus on the developmen

157 Essential to the pathogenesis of F. tularensis is its ability to escape the destructive p

158 The pathogenicity of F. tularensis depends on its ability to persist inside h

159 surface capsular and O-Ag polysaccharides of F. tularensis and initiates the classical complement cas

160 y, whole-genome transcriptional profiling of F. tularensis with DNA microarrays from infected tissues

161 This is the first report of F. tularensis FPI virulence proteins required for intram

162 ory role in the oxidative stress response of F. tularensis.

163 study identifies AIM2 as a crucial sensor of F. tularensis infection and provides genetic proof of it

164 r studies, using a virulent type A strain of F. tularensis (SchuS4), indicate that IL-17Ralpha(-/-) m

165 A REP34 knock-out strain of F. tularensis has a reduced ability to both induce encys

166 s study, the highly human virulent strain of F. tularensis SCHU S4 and the live vaccine strain were u

167 accine strain and virulent Schu S4 strain of F. tularensis to inhibit the proinflammatory response of

168 lenge with both type A and type B strains of F. tularensis and induced functional immunity through bo

169 Virulent strains of F. tularensis subsp. tularensis are devoid of classical,

170 s between attenuated and virulent strains of F. tularensis.

171 t respiratory infection by type A strains of F. tularensis.

172 ctivity differed among the subpopulations of F. tularensis and between the species.

173 h the intramacrophage growth and survival of F. tularensis.

174 ne hepatocytic cell line compared to that of F. tularensis cultured in broth.

175 the uptake and intracellular trafficking of F. tularensis Live Vaccine Strain (LVS) and LVS with dis

176 elp elucidate a mechanistic understanding of F. tularensis infection of phagocytic cells.

177 asked whether complement-dependent uptake of F. tularensis strain SCHU S4 affects the survival of pri

178 larly that of ferrous iron, for virulence of F. tularensis in the mammalian host.

179 Extreme infectivity and virulence of F. tularensis is due to its ability to evade immune dete

180 We propose that the extreme virulence of F. tularensis is partially due to the bifunctional natur

181 h crucial for normal growth and virulence of F. tularensis.

182 gs indicate that recognition of C3-opsonized F. tularensis, but not extensive cytosolic replication,

183 ted in concert for phagocytosis of opsonized F. tularensis by human neutrophils, whereas CR3 and CR4

184 ly inoculated with F. novicida U112, LVS, or F. tularensis Schu S4.

185 the presence of complement, whereas parental F. tularensis LVS is internalized within spacious pseudo

186 nce, and gene regulation of human pathogenic F. tularensis subspecies.

187 Because of its extreme pathogenicity, F. tularensis is classified as a category A bioweapon by

188 have now evaluated the lethality of primary F. tularensis live vaccine strain (LVS) pulmonary infect

189 CD4(+) T cells to the lungs after pulmonary F. tularensis LVS infection.

190 te processes in the lung following pulmonary F. tularensis infection and provide additional insight i

191 Importantly, pulmonary F. tularensis LVS infection of MR1-deficient (MR1(-/-))

192 the infected lungs, and control of pulmonary F. tularensis LVS growth.

193 We found that the lethality of pulmonary F. tularensis LVS infection was exacerbated under condit

194 s a vector for the expression of recombinant F. tularensis proteins.

195 Many of these mutations render F. tularensis defective for intracellular growth.

196 ve a critical protective role in respiratory F. tularensis LVS infection.

197 ld-type mice highly sensitive to respiratory F. tularensis infection, and depletion beginning at 3 da

198 trate here that AIM2 is required for sensing F. tularensis.

199 Here, we demonstrate a highly sensitive F. tularensis assay that incorporates sample processing

200 Despite the monomorphic nature of sequenced F. tularensis genomes, there is a significant degree of

201 Previously, we identified seven F. tularensis proteins that induce a rapid encystment ph

202 Gr-1(+) CD11b(+) cells in mice that survived F. tularensis infection also suggests a potential role f

203 gs of mice infected with the LVS rather than F. tularensis type A, while IL-23p19 mRNA expression was

204 S represses inflammasome activation and that F. tularensis-encoded FTL_0325 mediates this effect.

205 Here, we demonstrate that F. tularensis DsbA is a bifunctional protein that oxidiz

206 In summary, we demonstrate that F. tularensis profoundly impairs constitutive neutrophil

207 We now demonstrate that F. tularensis significantly inhibited neutrophil apoptos

208 Here we establish that F. tularensis limits Ca(2+) entry in macrophages, thereb

209 ur findings provide compelling evidence that F. tularensis catalase restricts reactive oxygen species

210 lectively, this study provides evidence that F. tularensis LVS represses inflammasome activation and

211 These findings further illustrate that F. tularensis LVS possesses numerous genes that influenc

212 The data also indicate that F. tularensis pathogenesis is controlled by a highly int

213 We demonstrated previously that F. tularensis inhibits NADPH oxidase assembly and activi

214 We also report that F. tularensis inhibits ROS-dependent autophagy to promot

215 rly infection has led to the suggestion that F. tularensis evades detection by host innate immune sur

216 This suggests that F. tularensis may possess specific factors that aid in e

217 The F. tularensis genome is predicted to encode 31 major fac

218 The F. tularensis subsp. tularensis DeltaFTT0798 and DeltaFT

219 nuated Listeria monocytogenes expressing the F. tularensis immunoprotective antigen IglC) as the boos

220 accharide antigen and 31 bacteria/mL for the F. tularensis bacteria were achieved.

221 DE-encoding protein genes are present in the F. tularensis genome.

222 We were particularly interested in the F. tularensis LVS (live vaccine strain) clpB (FTL_0094)

223 ate that AcpA, which contributes most of the F. tularensis acid phosphatase activity, is secreted int

224 and RNA-Seq we identify those regions of the F. tularensis chromosome occupied by PmrA and those gene

225 associates with 252 distinct regions of the F. tularensis chromosome, but exerts regulatory effects

226 erein we report the crystal structure of the F. tularensis FabI enzyme in complex with our most activ

227 identified TolC as a virulence factor of the F. tularensis live vaccine strain (LVS) and demonstrated

228 st by using unmarked deletion mutants of the F. tularensis live vaccine strain (LVS).

229 xperiments identified five substrates of the F. tularensis Lon protease (FTL578, FTL663, FTL1217, FTL

230 ator of the oxidative stress response of the F. tularensis LVS.

231 rtant clues for further understanding of the F. tularensis stress response and pathogenesis.

232 thereby contributing to the survival of the F. tularensis subsp. holarctica live vaccine strain (LVS

233 We hypothesized that the F. tularensis DeltapyrF strains may replicate in cells o

234 ogy revealed that the immune response to the F. tularensis mutant strains was significantly different

235 Intradermal inoculation with the F. tularensis live vaccine strain (LVS) results in a rob

236 growth, leading us to hypothesize that these F. tularensis mutants are attenuated because they induce

237 In contrast to F. tularensis subsp. novicida iclR mutants, LVS and Schu

238 results demonstrate that trpB contributes to F. tularensis virulence by enabling intracellular growth

239 ophages and other cell types are critical to F. tularensis pathogenesis, and impaired intracellular s

240 cinated rabbits were seropositive for IgG to F. tularensis lipopolysaccharide (LPS).

241 critical and novel regulator of immunity to F. tularensis LVS infection, its effects were masked dur

242 g the mechanisms that recruit neutrophils to F. tularensis-infected lungs, opsonization and phagocyto

243 F. novicida is closely related to F. tularensis and exhibits high virulence in mice, but i

244 FN-alpha and -beta) secretion in response to F. tularensis did not require AIM2.

245 sent in Aim2(-/-) macrophages in response to F. tularensis infection or the presence of cytoplasmic D

246 ch literature exists on the host response to F. tularensis infection, the vast majority of work has b

247 del of CR3 and TLR2 signaling in response to F. tularensis.

248 te to macrophage inflammation in response to F. tularensis.

249 a crucial role in innate immune responses to F. tularensis.

250 equired for macrophage cytokine responses to F. tularensis.

251 ungs of MAb-iFT-immunized mice subsequent to F. tularensis LVS challenge.

252 deficient mice were extremely susceptible to F. tularensis infection, with greater mortality and bact

253 L-17Ralpha(-/-) mice are more susceptible to F. tularensis LVS infection, our studies, using a virule

254 facultative anaerobe Francisella tularensis: F. tularensis subsp. tularensis (type A) and F. tularens

255 Analysis of wild-type F. tularensis isolates by DISA correlated with pulsed-fi

256 age growth that can be restored to wild-type F. tularensis LVS levels by either transcomplementation,

257 tive than the currently available unlicensed F. tularensis live vaccine strain (LVS) is needed to pro

258 onse against attenuated F. tularensis versus F. tularensis type A differs.

259 potent protective immunity against virulent F. tularensis SchuS4 challenge.

260 vival during pulmonary infection by virulent F. tularensis.

261 monstrate that lipids enriched from virulent F. tularensis strain SchuS4, but not attenuated live vac

262 role in infection mediated by fully virulent F. tularensis is not known.

263 doses (LD50) of aerosolized highly virulent F. tularensis Schu S4 had a significantly higher surviva

264 on, both F. novicida and the highly virulent F. tularensis subsp. tularensis Schu S4 strain are able

265 neumonic tularemia using the highly virulent F. tularensis subspecies tularensis SchuS4 strain and in

266 trophy is also important in a human-virulent F. tularensis subspecies.

267 to detect and distinguish the more virulent F. tularensis subsp. tularensis (subtypes A.I and A.II)

268 were infected with the prototypical virulent F. tularensis strain, Schu S4.

269 In this study, we demonstrate that virulent F. tularensis impairs production of inflammatory cytokin

270 In this study, we demonstrated that virulent F. tularensis strain SchuS4 selectively inhibits product

271 25 and its ortholog FTT0831c in the virulent F. tularensis SchuS4 strain in intramacrophage survival

272 of B1a cells in defense against the virulent F. tularensis ssp. tularensis strain SchuS4.

273 trolling survival of infection with virulent F. tularensis.

274 In vitro, F. tularensis invaded human erythrocytes, as shown in th

275 s of intraocular inflammation in areas where F. tularensis is endemic.

276 It is unknown, however, whether F. tularensis can infect erythrocytes; thus, we examined

277 fsl operon are the only major means by which F. tularensis acquires iron.

278 However, the molecular mechanisms by which F. tularensis DsbA contributes to virulence are unknown.

279 ore, we sought an alternative means by which F. tularensis might obtain iron.

280 The means by which F. tularensis modulates macrophage activation are not fu

281 Our understanding of the mechanisms by which F. tularensis senses and adapts to host environments is

282 li mviN, a putative lipid II flippase, which F. tularensis uses to evade activation of innate immune

283 lla factors and the mechanisms through which F. tularensis mediates these suppressive effects remain

284 unosensor formats for the detection of whole F. tularensis bacteria were developed and their performa

285 The severe morbidity associated with F. tularensis infections is attributed to its ability to

286 nged survival upon subsequent challenge with F. tularensis Schu S4 and provided complete protection a

287 mals treated with poly(I:C), challenged with F. tularensis, and then treated with LEVO 5 days later h

288 onses generated in macrophages infected with F. tularensis live vaccine strain (LVS) or the virulent

289 ved monocytes and neutrophils, infected with F. tularensis LVS ex vivo, display enhanced restriction

290 d on blood drawn from macaques infected with F. tularensis Schu S4 at daily intervals.

291 ified from the spleens of mice infected with F. tularensis suppressed polyclonal T-cell proliferation

292 ulation in the spleens of mice infected with F. tularensis.

293 nthetic pathway in macrophages infected with F. tularensis.

294 nd cytokine production during infection with F. tularensis live vaccine strain (LVS).

295 ve immunity against pulmonary infection with F. tularensis live vaccine strain, its production is tig

296 sed mortality after pulmonary infection with F. tularensis live vaccine strain.

297 nd pathology during pulmonary infection with F. tularensis live vaccine strain.

298 eased resistance to pulmonary infection with F. tularensis.

299 Using PBLs from mice vaccinated with F. tularensis Live Vaccine Strain (LVS) and related atte

300 mutant strains compared with wild-type (WT) F. tularensis LVS.