ライフサイエンスコーパス: C. neoformans

1 C. neoformans chemical-genetic responses are largely dis

2 C. neoformans expresses four putative CDAs, three of whi

3 C. neoformans has a defined a-alpha opposite sexual cycl

4 C. neoformans has the capacity to escape phagocytic cell

5 C. neoformans is a facultative intracellular microorgani

6 C. neoformans is unique among fungal pathogens in bearin

7 C. neoformans responded to oleic acid supplementation by

8 C. neoformans-induced lysosome damage was observed in in

9 gnature-tagged gene deletion strains for 155 C. neoformans TF genes has been established.

10 e and shedding were measured in vitro for 48 C. neoformans isolates.

11 We also engineered a C. neoformans strain that lacks UDP-galactopyranose muta

12 In a C. neoformans ccr4Delta mutant, stabilized ribosomal pro

13 erimental pulmonary infection of mice with a C. neoformans strain that induces protective immunity de

14 In contrast, pulmonary infection with a C. neoformans strain that secretes IFN-gamma, H99gamma,

15 ing less junctional diversity than acapsular C. neoformans-selected cells.

16 es in the environment coincidentally adapted C. neoformans for human virulence.

17 thesis that human immunoglobulins may affect C. neoformans virulence in vivo warrants further investi

18 Our data show human IgM affects C. neoformans morphology in vitro and suggest that the h

19 avage fluid from WT and SP-D(-/-) mice after C. neoformans infection.

20 pt for the echinocandins were active against C. neoformans, and the triazoles were active against oth

21 l)] displayed high in vitro activity against C. neoformans (IC50 = 0.35 mug/mL, MIC = MFC = 0.63 mug/

22 hat murine pDCs have direct activity against C. neoformans via reactive oxygen species (ROS), a mecha

23 o had decreased fungistatic activity against C. neoformans when activated.

24 K1-S1P pathway promotes host defense against C. neoformans infections by regulating cytokine levels,

25 nse provides a first line of defense against C. neoformans.

26 d cultured in vitro were fungistatic against C. neoformans, whereas cryptococcal growth was uncontrol

27 l enzymes, and mechanisms of killing against C. neoformans.

28 ties (MIC(80) and time-kill profile) against C. neoformans, and performed an extensive SAR study, whi

29 However, SP-D is not protective against C. neoformans.

30 hage autophagy plays different roles against C. neoformans, depending on the macrophage type and acti

31 itory concentration were synergistic against C. neoformans.

32 the cAMP/PKA and pH-sensing pathways allows C. neoformans to respond to a broad range of host-specif

33 Among C. neoformans-containing myeloid cells, recently recruit

34 The EA was lower for fluconazole and C. neoformans at 86.4%.

35 percent identities between the C. gattii and C. neoformans species complexes resulted in only a 74 to

36 ryptococcus species complexes, C. gattii and C. neoformans, which are the main pathogenic members of

37 selected B-1 B cells secreted laminarin- and C. neoformans-binding IgM.

38 ify factors associated with P. marneffei and C. neoformans admissions.

39 binding in C. neoformans-infected mice, and C. neoformans-selected B-1 B cells secreted laminarin- a

40 quired for M1 macrophage activation and anti-C. neoformans activity via the production of NO.

41 m by which M1 macrophages mediate their anti-C. neoformans activity remains unknown.

42 ins, CnMVs are distributed inside and around C. neoformans-induced cystic lesions.

43 udies suggested that the interaction between C. neoformans hyaluronic acid and human brain endothelia

44 MARCO facilitates early interactions between C. neoformans and lung-resident cells and promotes the p

45 the importance of the interrelation between C. neoformans and the brain endothelium in establishing

46 t MLST-derived genotype similarities between C. neoformans strains do not necessarily translate into

47 lls, which express germline V(H) genes, bind C. neoformans and contribute to early fungal clearance.

48 roscopy showed normal human IgG and IgM bind C. neoformans (ii) C. neoformans grown in titan cell-ind

49 and arrangement of melanin pigments in both C. neoformans and C. gattii species complexes.

50 ased the frequency of lipid droplets in both C. neoformans and macrophages.

51 lizes Cu as an innate antifungal defense but C. neoformans senses and neutralizes toxic Cu to promote

52 cell-wall components of invading fungi, but C. neoformans can circumvent this immunosurveillance mec

53 o understand macrophage pathways affected by C. neoformans toxicity.

54 raversal of the blood-brain barrier (BBB) by C. neoformans invitro.

55 ide with rapid fungicidal activity caused by C. neoformans.

56 blood-brain barrier adhesion and crossing by C. neoformans.

57 , our data show that SRA can be exploited by C. neoformans to interfere with the early events of the

58 Infection of macrophages by C. neoformans was associated with alterations in protein

59 ls exhibited the most acapsular and capsular C. neoformans binding in C. neoformans-infected mice, an

60 )12, respectively, in acapsular and capsular C. neoformans-selected B-1a cells.

61 mline V(H) segments were used, with capsular C. neoformans-selected cells having less junctional dive

62 ces of this challenge, we have characterized C. neoformans GMP synthase, the second enzyme in the gua

63 Neutrophils were directly seen to chase C. neoformans cells and then rapidly internalize them.

64 was found in only a few vacuoles containing C. neoformans previously opsonized with antibody but nev

65 sa1, significantly contributes to serotype D C. neoformans virulence through the induction of laccase

66 udate macrophages in the lungs and decreased C. neoformans-specific Th2 cells in the mediastinal lymp

67 eraction, we utilized a previously described C. neoformans mutant, the gpr4Delta gpr5Delta mutant, wh

68 cryptococci seen in mammalian cells despite C. neoformans being able to grow at bird body temperatur

69 that SIS is conserved between the divergent C. neoformans serotype A and serotype D cryptic sibling

70 MARCO in activation of the CCR2 axis during C. neoformans infection.

71 The protective response induced during C. neoformans strain H99gamma (C. neoformans strain H99

72 and SK1-S1P pathway are interrelated during C. neoformans infections.

73 lacking SP-D were partially protected during C. neoformans infection; they displayed a longer mean ti

74 was performed using a Caenorhabditis elegans-C. neoformans infection assay.

75 , which we conclude functions as the elusive C. neoformans pheromone-response factor.

76 sly reported the generation of an engineered C. neoformans strain (C. neoformans Deltagcs1) which can

77 CnMVs also enhanced C. neoformans infection of the brain, found in both infe

78 METH enhances C. neoformans pulmonary infection, facilitating its diss

79 biased lung immunopathology that facilitates C. neoformans growth and dissemination.

80 Sixty-five C. neoformans isolates from clinical trial patients with

81 E] and 2.6% major errors [ME]) and 84.1% for C. neoformans (4.5% VME and 11.4% ME).

82 In this study, occurrence data for C. neoformans and C. gattii were compared by MaxEnt soft

83 ere 9.1 h for Candida species and 12.1 h for C. neoformans.

84 ructural information, we propose a model for C. neoformans' melanization that is similar to the proce

85 ent a genome-scale co-functional network for C. neoformans, CryptoNet, which covers ~81% of the codin

86 Both IgE and IgA were opsonic for C. neoformans and protected against infection in mice.

87 n the environment in purine-rich bird guano, C. neoformans experiences a drastic change in nutrient a

88 nduced during C. neoformans strain H99gamma (C. neoformans strain H99 engineered to produce murine IF

89 al human IgG and IgM bind C. neoformans (ii) C. neoformans grown in titan cell-inducing medium with I

90 e compared plasma levels of immunoglobulins, C. neoformans glucuronoxylomannan (GXM) capsule-specific

91 induction of lysosome damage is an important C. neoformans survival strategy and that classical activ

92 In C. neoformans, the pigment associates with key cellular

93 In C. neoformans, this adaptation is accompanied by Ccr4-me

94 gly, meiosis-specific genes are activated in C. neoformans and contribute to ploidy reduction, both i

95 show that this protein plays a role also in C. neoformans infection.

96 psular and capsular C. neoformans binding in C. neoformans-infected mice, and C. neoformans-selected

97 e model to explore the importance of CD44 in C. neoformans brain invasion.

98 that mRNA synthesis and decay are coupled in C. neoformans via Rpb4, and this tight coordination prom

99 rs governing cell-wall pigment deposition in C. neoformans and C. gattii.

100 ell formation is a novel virulence factor in C. neoformans that promotes establishment of the initial

101 Increased lysosome damage was found in C. neoformans-containing lung cells compared with C. neo

102 have identified a kinase that is involved in C. neoformans internalization by host cells and in host

103 Lastly, we found that MARCO was involved in C. neoformans phagocytosis by resident pulmonary macroph

104 ng confirmed Ipk1 as the major IP5 kinase in C. neoformans: ipk1Delta produced no IP6 or PP-IP5/IP7 a

105 e, we report that ADE13 encodes ADS lyase in C. neoformans.

106 TP, prompting us to investigate ADS lyase in C. neoformans.

107 characterized by generating null mutants in C. neoformans.

108 on would improve immunological parameters in C. neoformans-infected TLR9(-/-) mice.

109 cient replication of methylation patterns in C. neoformans, rare stochastic methylation loss and gain

110 ranscription factor is uniquely regulated in C. neoformans both by the canonical pH-sensing pathway a

111 mechanisms of oxidative stress resistance in C. neoformans.

112 tin may have a potential therapeutic role in C. neoformans infections of the brain.

113 s are important for radiation sensitivity in C. neoformans by regulating specific downstream AAP gene

114 We also found that PS synthase in C. neoformans is localized to the endoplasmic reticulum

115 uptake is a potential therapeutic target in C. neoformans.

116 he concept of dormancy has been validated in C. neoformans from both epidemiological and genotyping d

117 etworks that control growth and virulence in C. neoformans.

118 ental induction of lysosome damage increased C. neoformans replication.

119 of lysosome damage correlated with increased C. neoformans replication.

120 In immunocompromised individuals, C. neoformans can lead to life-threatening meningoenceph

121 reproduce in vivo conditions that influence C. neoformans virulence.

122 together, our results show that pDCs inhibit C. neoformans growth in vitro via the production of ROS

123 ely 800 macrophages containing intracellular C. neoformans and identified 163 nonlytic exocytosis eve

124 totoxic effect associated with intracellular C. neoformans residence that manifested itself in impair

125 t macrophages display little ability to kill C. neoformans in vitro.

126 the oxidative burst inside the macrophages, C. neoformans has developed multilayered redundant molec

127 wild type in the insect Galleria mellonella-C. neoformans infection assay.

128 Cryptococcus neoformans (C. neoformans var. grubii) is an environmentally acquire

129 cell division in the presence or absence of C. neoformans infection.

130 stingly, the metabolic pathway adaptation of C. neoformans to H(2)O(2) treatment was remarkably disti

131 wall changes required for the adaptation of C. neoformans to its host environment.

132 etics, and cellular and molecular biology of C. neoformans have dramatically improved our understandi

133 CRIg but not CR3, are involved in capture of C. neoformans.

134 Infection of BALB/c mice with 10(4) CFU of C. neoformans H99 caused a time-dependent induction of I

135 the pathobiological signalling circuitry of C. neoformans and identifies potential anticryptococcal

136 the pathobiological signalling circuitry of C. neoformans.

137 mary outcome of the rate of CSF clearance of C. neoformans over the subsequent 4 weeks was compared.

138 ent of HIV/CM would improve CSF clearance of C. neoformans.

139 lence traits to evaluate the contribution of C. neoformans phenotypic diversity to clinical presentat

140 nd subsequently impaired adaptive control of C. neoformans in the infected lungs.

141 Successful control of C. neoformans infection is dependent on host macrophages

142 hile macrophages are critical for control of C. neoformans, a failure of macrophage response is not t

143 age polarization, limiting innate control of C. neoformans, but ultimately has no effect on cryptococ

144 we describe in this review the life cycle of C. neoformans with a special emphasis on the regulation

145 ear fragmentation and membrane disruption of C. neoformans cells.

146 tics resources for the genetic dissection of C. neoformans phenotypes.

147 ckade effectively abrogated dissemination of C. neoformans to the brain.

148 esults demonstrate a new cytotoxic effect of C. neoformans infection on murine macrophages: fungus-in

149 cells also decreased nonlytic exocytosis of C. neoformans, increased interleukin-6 secretion, and de

150 Following phagocytosis, the growth of C. neoformans is inhibited by KCs in an IFN-gamma indepe

151 Finally we showed the importance of C. neoformans Srx1 in fungal pathogenesis by demonstrati

152 Recently, we reported that ingestion of C. neoformans by mouse macrophages induces early cell cy

153 Internalization of C. neoformans by KCs is subsequently mediated by multipl

154 702 isolates, 13 species) and 44 isolates of C. neoformans against fluconazole.

155 In diploid isolates of C. neoformans var. grubii (serotype AA) and of hybrids w

156 While most isolates of C. neoformans var. grubii belong to one of three major l

157 lular recognition, ingestion, and killing of C. neoformans and discuss the unique and remarkable feat

158 C5a-C5aR signaling in neutrophil killing of C. neoformans in real time.

159 TES and more efficient uptake and killing of C. neoformans These findings suggest that DAP12 acts as

160 some damage and enabled increased killing of C. neoformans.

161 phil migration and its subsequent killing of C. neoformans.

162 tion alters the transcriptional landscape of C. neoformans with the result of increased resistance to

163 augmented understanding of the mechanisms of C. neoformans melanin biosynthesis and cellular assembly

164 ular interactions underlying melanization of C. neoformans have yielded to comprehensive molecular-sc

165 Using a mouse model of C. neoformans infection, we demonstrated that MARCO defi

166 In commonly used mouse models of C. neoformans infections, fungal cells are not contained

167 In this study, we used time-lapse movies of C. neoformans-infected macrophages to delineate the kine

168 e, consistent with the nonspecific nature of C. neoformans virulence known to infect phylogenetically

169 whereby this molecule affects the outcome of C. neoformans infection by inhibiting fungal growth and

170 cient method of studying the pathogenesis of C. neoformans.

171 ts in our lab had shown that phagocytosis of C. neoformans promoted cell cycle progression.

172 and less alveolar macrophage phagocytosis of C. neoformans than did control and B-1a B cell-reconstit

173 Consistent with this, phosphorylation of C. neoformans Hog1 was modulated by both low and high do

174 The phylogeny of C. neoformans reveals a recent exponential population ex

175 a unique, genetically diverse population of C. neoformans from sub-Saharan Africa, commonly isolated

176 have elucidated the virulence properties of C. neoformans, less is understood regarding lung host im

177 AD1 expression reduces innate recognition of C. neoformans, rendering the yeast resistant to eliminat

178 d HOG1, genes encoding central regulators of C. neoformans stress response pathways and cell morphoge

179 verning pathogenicity and drug resistance of C. neoformans is imperative.

180 cess in understanding the stress response of C. neoformans and for understanding fungal physiology.

181 of melanin on the transcriptomic response of C. neoformans to gamma radiation.

182 ss the BBB and accumulate at lesion sites of C. neoformans-infected brains.

183 with a highly virulent serotype A strain of C. neoformans (H99).

184 a moderately virulent encapsulated strain of C. neoformans (strain 52D).

185 Studies using a virulent strain of C. neoformans engineered to produce gamma interferon (IF

186 onstrate that a Deltaplb1 knockout strain of C. neoformans has a profound defect in intracellular gro

187 ic infection with a high-virulence strain of C. neoformans significantly induced pulmonary IL-25 expr

188 A mutant strain of C. neoformans that cannot transport xylose precursors in

189 nses against a moderately virulent strain of C. neoformans through effects on leukocyte recruitment,

190 11% of the patients infected with strains of C. neoformans var. grubii with identical genotypes exhib

191 Supplementation of C. neoformans and macrophages with oleic acid significan

192 essential for dissemination and survival of C. neoformans in a host environment was compromised even

193 C. gattii capsules were larger than those of C. neoformans (P < 0.001).

194 ug resistance response upon the treatment of C. neoformans with H(2)O(2).

195 case trafficking and attenuates virulence of C. neoformans in a mouse intravenous (i.v.) meningitis m

196 ys important for the growth and virulence of C. neoformans.

197 l growth and exerts a direct lytic effect on C. neoformans extracellular vesicles (EVs).

198 mined the effect of human immunoglobulins on C. neoformans titan cell formation in vitro (i) Fluoresc

199 mice infected with either strain H99gamma or C. neoformans strain 52D (unmodified clinical isolate).

200 Dendritic cells (DCs) phagocytose C. neoformans following inhalation.

201 We sequenced 699 isolates, primarily C. neoformans from HIV-infected patients, from 5 countri

202 lity to C. neoformans infection by promoting C. neoformans-driven pulmonary IL-5 and eosinophil infil

203 lmonary surfactant protein D (SP-D) protects C. neoformans cells against macrophage-mediated defense

204 stent with the upregulation of Cmt proteins, C. neoformans pulmonary infection results in increased s

205 monstrated that protection against pulmonary C. neoformans infection is associated with the generatio

206 ide a first line of defense during pulmonary C. neoformans infection in mice.

207 We determined that pulmonary C. neoformans infection results in Cu-specific induction

208 eptors on host phagocytes known to recognize C. neoformans Altogether, we have identified a kinase th

209 Purified recombinant C. neoformans ADS lyase shows catalytic activity similar

210 lls, DAP12(-/-) NK cells are able to repress C. neoformans growth in vitro Additionally, DAP12(-/-) m

211 to its role in peroxide sensing and response C. neoformans Srx1 was also found to be required for a p

212 vated ATG5-knockout BMMs actually restricted C. neoformans growth more efficiently, suggesting that m

213 survival time was not associated with single C. neoformans virulence factors in vitro or in vivo; rat

214 strated that the aliphatic moieties of solid C. neoformans melanin ghosts include cell-wall component

215 s the ability of birds to efficiently spread C. neoformans in the environment whilst avoiding systemi

216 ation of an engineered C. neoformans strain (C. neoformans Deltagcs1) which can be contained in lung

217 In summary, C. neoformans harvests lipids from macrophages, and the

218 We show that in the absence of GMP synthase, C. neoformans becomes a guanine auxotroph, the productio

219 Besides serving as an antimicrobial target, C. neoformans ADS lyase inhibitors may also serve as pot

220 solates exhibited a wider range of MICs than C. neoformans.

221 These findings demonstrate that C. neoformans lipids are more varied compositionally and

222 This is the first demonstration that C. neoformans-derived microvesicles can facilitate crypt

223 In this study, we found that C. neoformans-derived microvesicles (CnMVs) can enhance

224 Thus, our data highlight that C. neoformans, a human-pathogenic basidiomycete, has evo

225 Our results indicate that C. neoformans infection impairs multiple host cellular f

226 It is well known that C. neoformans generally affects immunocompromised hosts;

227 globulins are part of the immune milieu that C. neoformans confronts in a human host, and its ability

228 yclophilin A further support the notion that C. neoformans elicits changes in brain endothelial cells

229 Here, we report that C. neoformans infection with highly virulent and less vi

230 In this study, we report that C. neoformans rapidly and transiently repressed ribosoma

231 psule, and stress response genes showed that C. neoformans grown with IgM, not IgG or phosphate-buffe

232 Our results showed that C. neoformans-infected CD44 KO mice survived longer than

233 The C. neoformans HOG (High Osmolarity Glycerol response) pa

234 The C. neoformans isolates were collected within clinical tr

235 The C. neoformans SRP RNA displays a predicted structure in

236 melanization itself dramatically altered the C. neoformans transcriptome, primarily by repressing gen

237 ns harvests lipids from macrophages, and the C. neoformans-macrophage interaction is modulated by exo

238 differences in substrate binding between the C. neoformans and human enzymes, with structural insight

239 dentified and functionally characterized the C. neoformans pheromone-response element (PRE).

240 In contrast, the C. neoformans var. neoformans map was completely differe

241 amino acid differences are identified in the C. neoformans crystal structure, in particular a threoni

242 a sex-induced silencing (SIS) pathway in the C. neoformans serotype A var. grubii lineage, in which t

243 exploring the evolution of virulence in the C. neoformans-C. gattii clade.

244 ion maps of the species and varieties of the C. neoformans and C. gattii species complex in Europe an

245 application to study the architecture of the C. neoformans capsule under a variety of conditions.

246 Indeed, additional removal of the C. neoformans H3K9 methyltransferase Clr4 results in los

247 ous phenome-based functional analysis of the C. neoformans TF mutant library identified key TFs impor

248 our phenome-based functional analysis of the C. neoformans TF mutant library provides key insights in

249 n has been driven by three sub-clades of the C. neoformans VNIa lineage; VNIa-4, VNIa-5 and VNIa-93.

250 tylation of chitosans already exposed on the C. neoformans cell wall (originally produced by CnChs3 a

251 spite its divergent upstream regulation, the C. neoformans Rim101 protein recognizes a conserved DNA

252 ogy is a promising approach for studying the C. neoformans capsule and its associated polysaccharides

253 This study used the C. neoformans requirement of exogenous obligatory catech

254 Immunoblot analysis using the C. neoformans Tsa1 specific antibody revealed that both

255 -17 axis after intranasal infection with the C. neoformans strain 52D.

256 o the levels found in mice infected with the C. neoformans wild type, and their levels were also depe

257 Deltagcs1 but not in mice infected with the C. neoformans wild type.

258 Thus, C. neoformans produces an autoregulatory peptide that ma

259 and sufficient for neutrophils to attach to C. neoformans but was unable to mediate phagocytosis.

260 that these organelles could be connected to C. neoformans melanin synthesis.

261 cells in the presence of a specific IgG1 to C. neoformans capsular polysaccharide.

262 the role of STAT1 in protective immunity to C. neoformans is unknown.

263 n in murine models of protective immunity to C. neoformans.

264 hermore, susceptibility of SP-D(-/-) mice to C. neoformans infection could be restored to the level o

265 IgA reactivity to C. neoformans and A. fumigatus was greater in the BALF o

266 ffei admissions were more common relative to C. neoformans admissions during months of high (>/=85%)

267 a brake on the pulmonary immune response to C. neoformans by promoting pulmonary eosinophilia and by

268 nt inhibitory role in the immune response to C. neoformans Infectious outcomes in DAP12(-/-) mice, in

269 we examined the role of SP-D in response to C. neoformans using SP-D(-)/(-) mice.

270 role played by SP-D during host responses to C. neoformans and consequently imparts insight into pote

271 othesized that SP-D alters susceptibility to C. neoformans by dysregulating the innate pulmonary immu

272 lusion that SP-D increases susceptibility to C. neoformans infection by promoting C. neoformans-drive

273 ce manifested no increased susceptibility to C. neoformans, as measured by survival, but had fewer al

274 ary eosinophilia and are more susceptible to C. neoformans infection than WT mice.

275 t affect the migration of neutrophils toward C. neoformans but almost completely abolished phagocytos

276 during the protective response to wild-type C. neoformans in mice previously immunized with H99gamma

277 y protected against challenge with wild-type C. neoformans.

278 odel of inhalational infection with virulent C. neoformans H99, we demonstrate a role for IL-33-depen

279 rom ionizing radiation damage, against which C. neoformans is extremely resistant.

280 id profiles were remarkably similar in whole C. neoformans cells, grown under either melanizing or no

281 e mastermind-like within mature T cells with C. neoformans Inhibition of T cell-restricted Notch sign

282 uman brain endothelial cells challenged with C. neoformans was resolved using a label-free differenti

283 tionally high chitosan content compared with C. neoformans H99; a rich chitosan composition promoted

284 Compared with C. neoformans MICs, C. gattii MICs were lower for flucyt

285 oformans-containing lung cells compared with C. neoformans-free cells.

286 ar. grubii (serotype AA) and of hybrids with C. neoformans var. neoformans (serotype AD) such aneuplo

287 Incubation with C. neoformans resulted in enhanced activation of Erk and

288 eolar lavage fluid of all mice infected with C. neoformans Deltagcs1 but not in mice infected with th

289 r alpha were found in the mice infected with C. neoformans Deltagcs1 in comparison to the levels foun

290 2-deficient (T1/ST2(-/-)) mice infected with C. neoformans H99 had improved survival with a decreased

291 ating that SP-D-deficient mice infected with C. neoformans have a lower fungal burden and live longer

292 f eosinophils and/or IL-5 were infected with C. neoformans to assess the role of these innate immune

293 pidly than wild-type mice when infected with C. neoformans, and Anxa2(-/-) mice exhibited enhanced in

294 B cell response to pulmonary infection with C. neoformans and reveal that IgM-producing B-1a cells,

295 rent studies demonstrate that infection with C. neoformans strain H99gamma in mice with macrophage-sp

296 mpared to wild-type mice upon infection with C. neoformans This increase in survival correlated with

297 led analysis of macrophage interactions with C. neoformans during infection.

298 -/-) mice were infected intratracheally with C. neoformans.

299 the dynamic interactions of neutrophils with C. neoformans and the underlying mechanisms in real time

300 the dynamic interactions of neutrophils with C. neoformans, demonstrating a crucial role of C5a-C5aR