ライフサイエンスコーパス: filarial

1 dependent pathways are sufficient to control filarial adult infection via an eosinophil-dependent eff

2 (Uninf) subjects following stimulation with filarial Ag (BmA) or with the M. tuberculosis-specific A

3 e the relationship between early exposure to filarial Ag and subsequent immune responsiveness, CD45RA

4 Upon stimulation with filarial Ag, a diminished up-regulation of TLR was obser

5 rnal infection status did not correlate with filarial Ag-driven IL-2, IFN-gamma, IL-4, or IL-5 respon

6 In contrast, filarial Ag-driven IL-5 production was 5.5-fold greater

7 xhibit significantly expanded frequencies of filarial Ag-induced Th9 cells, but not of IL9(+)Th2 cell

8 requently than CD4(+) T cells in response to filarial Ag.

9 wer proliferation and IFN-gamma responses to filarial Ags, nonparasite Ag, and PHA by PBMC compared w

10 wever, the role of early innate responses to filarial and Wolbachia ligands in the development of fil

11 ongoing infection (positive for circulating filarial antigen [CFA]), or whether the majority of CFA-

12 patent filarial infections are studded with filarial antigen and express markers associated with alt

13 ilariae-infected individuals stimulated with filarial antigen following IL-19 or IL-24 neutralization

14 as determined by whether in utero priming to filarial antigen occurs, is a major determinant of child

15 ial infection, as ascertained by circulating filarial antigen, relative to children of uninfected mot

16 infection present during gestation, with no filarial antigen-driven cord blood T cell response [n =

17 and were assayed for filarial infection and filarial antigen-driven interferon (IFN)- gamma , interl

18 esenting cell function and downmodulation of filarial antigen-specific T cell responses.

19 At the same timepoint, filarial antigenaemia in the doxycycline group fell to a

20 The relationship between filarial antigenemia and lymphatic pathology was investi

21 determined by blood-borne microfilariae and filarial antigenemia.

22 with a diagnosis of W. bancrofti circulating filarial antigens (CFAs) and 44 who also had microfilari

23 Phage expressing two filarial antigens (TCTP and BmALT-2) reacted with 1E9.

24 support the notion that in utero exposure to filarial antigens affects the natural history of filaria

25 individuals with intact immune responses to filarial antigens are capable of dealing with filarial e

26 mechanisms that lead to this Th2 bias toward filarial antigens are not clear, but one possibility is

27 then screened a novel expression library of filarial antigens displayed on the surface of T7 bacteri

28 irculation, which are chronically exposed to filarial antigens in infected subjects-is yet to be unde

29 ose of filariasis-infected subjects; whereas filarial antigens mediate apoptosis of normal human mono

30 rated that the classical subset internalized filarial antigens more efficiently than the other two su

31 feron [IFN]-gamma and interleukin [IL]-5) to filarial antigens were measured in 14 subjects with sero

32 mal monocytes, presumably due to circulating filarial antigens, and resulted in inhibition of PHA-ind

33 esults suggest that the role of Wolbachia in filarial biology is more subtle than previously thought

34 rculating microfilariae (mf) and presence of filarial biomarkers in sera occur following experimental

35 ated with systemic inflammatory reactions to filarial chemotherapy.

36 tified as a potent and specific inhibitor of filarial chitinases, an activity not previously reported

37 yclophilin shares 43-46% similarity to other filarial cyclophilins but does not belong to any of the

38 ls from 27 individuals either with lymphatic filarial disease (lymphedema), with the asymptomatic or

39 re involved in the pathogenesis of lymphatic filarial disease and that trafficking of particular cell

40 anti-Wolbachia immune responses and chronic filarial disease in humans, antibody responses to Wolbac

41 The pathogenesis of filarial disease is characterized by acute and chronic i

42 the role of the bacteria in worm biology or filarial disease is still not clear.

43 s a potential trigger for the development of filarial disease.

44 of lymphedema (and presumed inflammation) in filarial-diseased individuals.

45 and Wolbachia ligands in the development of filarial diseases has not been fully elucidated.

46 a narrower spectrum would aid in eliminating filarial diseases.

47 0.4% (P=0.005), and the rate of detection of filarial DNA decreased from 19.4% to 14.9% (P=0.13).

48 rgeting wBm is a promising approach for anti-filarial drug development.

49 generated a set of hybridomas reactive with filarial E/S products and screened them for their abilit

50 ic albendazole (ABZ) and drugs depleting the filarial endosymbiont Wolbachia, a proven macrofilaricid

51 ilarial antigens are capable of dealing with filarial exposure without developing persistent infectio

52 Similarly, these cytokines were induced by filarial extracts containing Wolbachia organisms but not

53 phage migration to the cornea in response to filarial extracts containing Wolbachia was dependent on

54 Wolbachia containing filarial extracts stimulated cytokine production in macr

55 or corneal fibroblasts, either alone or with filarial extracts; in contrast, rIFN-gamma was found to

56 ions, and coincident allergic sensitization (filarial [Fil](+)allergy [A](+)) were compared with the

57 host factors involved in the pathogenesis of filarial-induced diseases is paramount.

58 ow cytometry on PBMCs from 25 microfilaremic filarial-infected (Inf) and 14 filarial-uninfected (Unin

59 IgG, and IgG(4) antibodies were measured in filarial-infected and filarial-uninfected patients.

60 population, we performed ImmunoCAP tests in filarial-infected and noninfected individuals for IgE me

61 s significantly diminished in the T cells of filarial-infected individuals based on decreased T cell

62 R9 was significantly lower in T cells of the filarial-infected individuals compared with the uninfect

63 ut not of IL9(+)Th2 cells in comparison with filarial-infected individuals without associated disease

64 il(+); n = 19) and those without evidence of filarial infection (Fil(-); n = 19).

65 annually to age 7 years and were assayed for filarial infection and filarial antigen-driven interfero

66 macrophage function is down modulated during filarial infection and suggest that mechanisms involved

67 eosinophil tissue recruitment during chronic filarial infection and that IL-4R-independent/IL-5- and

68 We evaluated the status of filarial infection and the presence of W. bancrofti DNA

69 This work suggests that during filarial infection CTLA-4 coinhibition and CD4+ CD25+ Tr

70 ng malaria-infected individuals, concomitant filarial infection diminishes dramatically the frequenci

71 that allergic sensitization coincident with filarial infection drives parasite Ag-specific T cell hy

72 t individuals with pathology associated with filarial infection exhibit significantly expanded freque

73 Monocyte dysfunction in filarial infection has been proposed as one mechanism un

74 We found that having a tissue-invasive filarial infection increased the serological prevalence

75 These data indicate that maternal filarial infection increases childhood susceptibility to

76 Our data suggest that filarial infection induces Ag-specific, exaggerated IL-4

77 Filarial infection is initiated by mosquito-derived thir

78 In addition, filarial infection is likely detrimental to flight due t

79 the protective potential of T lymphocytes in filarial infection is well documented, investigation of

80 t to restore "normal" immune responsiveness; filarial infection may induce very long-term deficits in

81 agnostic biomarkers and drug targets for the filarial infection of humans.

82 the ages of 2 and 17 years were examined for filarial infection status as determined by blood-borne m

83 esence of chronic filarial morbidity and not filarial infection status in humans and suggest that WSP

84 These data indicate that chronic filarial infection suppresses eosinophilic responses to

85 Filarial infection was also associated with a marked inc

86 omparison with filarial-uninfected subjects, filarial infection was associated with higher ex vivo fr

87 Filarial infection was associated with IgE, IgG, and IgG

88 response to malaria Ag stimulation, however, filarial infection was associated with lower frequencies

89 Importantly, filarial infection was associated with markedly lower fr

90 cts on host clinical and immune responses to filarial infection, along with potential confounding det

91 factors in impaired Th1 responses of patent filarial infection, analysis of cytokine, SOCS, and tran

92 s had a three- to fourfold increased risk of filarial infection, as ascertained by circulating filari

93 In previous studies using a murine model of filarial infection, granuloma formation was found to be

94 Immune modulation is a hallmark of patent filarial infection, including suppression of antigen-pre

95 lationship, especially immunopathogenesis of filarial infection, may improve our understanding.

96 with the asymptomatic or subclinical form of filarial infection, or without filarial infection.

97 BL-A(-/-) mice or the effect was specific to filarial infection, we immunized these mice with OVA or

98 memory T cell compartments in the context of filarial infection, we used multiparameter flow cytometr

99 BmALT-2 is a potential vaccine candidate for filarial infection.

100 cific T cell unresponsiveness seen in patent filarial infection.

101 g/ml; p = 0.006) compared with those without filarial infection.

102 l hyporesponsiveness in patients with patent filarial infection.

103 nical form of filarial infection, or without filarial infection.

104 monocytes being expanded (almost 2-fold) in filarial infection.

105 mononuclear cells (PBMC) from patients with filarial infections (n=24) and from unexposed control su

106 The diagnosis of filarial infections among individuals residing in areas

107 tions in the circulation of 23 patients with filarial infections and 8 uninfected control subjects.

108 of 38 serum samples from patients with other filarial infections and for 1 of 23 serum samples from p

109 ssed using PBMC from 20 patients with active filarial infections and from 9 uninfected subjects.

110 h parasitologically proven S. stercoralis or filarial infections and from healthy, uninfected control

111 reds of millions of people annually to treat filarial infections and prevent elephantiasis.

112 Thus, PBMC from persons with filarial infections appear to have enhanced susceptibili

113 he most frequent producers of IL-10 in human filarial infections are CD4(+) T cells, many of which ar

114 Human monocytes from patients with patent filarial infections are studded with filarial antigen an

115 The global efforts for eliminating filarial infections by mass drug administration programs

116 Thus, the posttreatment reactions seen in filarial infections can be divided into an early phase w

117 , as such, may be useful in the treatment of filarial infections caused by Onchocerca volvulus, resul

118 Filarial infections evoke exuberant inflammatory respons

119 Filarial infections have been associated with the develo

120 factors in determining the host response to filarial infections in humans and emphasize the complexi

121 poptosis observed in vitro extends to patent filarial infections in humans and is reflected in the nu

122 te the utility of the molecular diagnosis of filarial infections in mobile populations.

123 suggest that in helminth infections (and in filarial infections in particular), the ratios of polycl

124 n extracellular parasitic infections such as filarial infections is not well-defined.

125 Together, these data demonstrate that filarial infections modulate the Plasmodium falciparum-s

126 Filarial infections of humans cause some of the most imp

127 The effect of filarial infections on malaria-specific immune responses

128 Basophil contribution to the IL-4 pool in filarial infections was assessed using PBMC from 20 pati

129 CD4(+) T cell responses in 12 subjects with filarial infections, and coincident allergic sensitizati

130 accharides modulates host immune response in filarial infections, this in vitro system may help in ga

131 To investigate the role of NK cells in filarial infections, we have used an in vitro model syst

132 patients undergoing evaluation for suspected filarial infections.

133 7 CD4(+) cells are expanded in vivo in human filarial infections.

134 and were susceptible to chronic fecund adult filarial infections.

135 important role in determining the outcome of filarial infections.

136 responsible for most immune dysregulation in filarial infections.

137 redominant cellular source of IL-10 in human filarial infections.

138 is a quintessential feature of chronic human filarial infections.

139 genesis of lymphatic lesions associated with filarial infections.

140 rophils and involved in host defense against filarial infections.

141 e for the surveillance of these understudied filarial infections.

142 e nature of the human B cell response during filarial infections.

143 ) are cytokines that are highly expressed in filarial infections.

144 d with the modulation of T-cell responses in filarial infections.

145 ials to assess its efficacy in patients with filarial infections.

146 rasite interactions during early third-stage filarial larva (L3) migration are poorly understood.

147 d as an improved tool to manage morbidity in filarial LE.

148 tudy was to determine whether improvement of filarial lymphedema (LE) by doxycycline is restricted to

149 ream, but is often ineffective to kill adult filarial (macrofilariae) in the complex anatomy of the l

150 Recently developed filarial molecular diagnostic assays are highly sensitiv

151 To understand further the filarial/monocyte interface, in vitro modeling demonstra

152 are associated with the presence of chronic filarial morbidity and not filarial infection status in

153 ining glycoprotein secreted by the parasitic filarial nematode Acanthocheilonema viteae targets dendr

154 62, a glycoprotein secreted by the parasitic filarial nematode Acanthocheilonema viteae, subverts hos

155 y of lymphocytes to respond appropriately to filarial nematode antigens and, in some cases, to other

156 wn, this study clearly demonstrates that the filarial nematode B. malayi is capable of transporting e

157 The filarial nematode Brugia malayi represents a leading cau

158 , named Bm-spn-2, has been isolated from the filarial nematode Brugia malayi, a causative agent of hu

159 ure and sequence four Wolbachia genomes: the filarial nematode Brugia malayi, wBm, (21-fold enrichmen

160 Heme acquisition in the parasitic filarial nematode Brugia malayi.

161 hsp83 was cloned from the filarial nematode Brugia pahangi.

162 unity can play a pivotal role in restricting filarial nematode development and suggest that genetical

163 or mediators of inflammatory pathogenesis in filarial nematode disease.

164 e source code, and (ii) a collection of four filarial nematode genomes.

165 e found in a wide diversity of arthropod and filarial nematode hosts.

166 evolved as essential endosymbionts of their filarial nematode hosts.

167 ng a well-characterized mouse model of human filarial nematode infection, nematode survival and prote

168 reported that in the context of experimental filarial nematode infection, optimum tissue eosinophil r

169 Filarial nematode infections cause a substantial global

170 ponses that limit the parasite burden during filarial nematode infections.

171 us on using anti-Wolbachia therapies against filarial nematode infections.

172 role, in chronic infection of mice with the filarial nematode L. sigmodontis.

173 Here, we engineered larvae of the filarial nematode Litomosoides sigmodontis as a vaccine

174 We further identify miRNAs from the filarial nematode Litomosoides sigmodontis in the serum

175 by investigating whether infection with the filarial nematode Litomosoides sigmodontis prevents diab

176 Infection with the parasitic filarial nematode Onchocerca volvulus can lead to severe

177 The filarial nematode Onchocerca volvulus is the causative o

178 s a neglected tropical disease caused by the filarial nematode Onchocerca volvulus that affects more

179 ous neglected tropical disease caused by the filarial nematode Onchocerca volvulus that can lead to b

180 symbiotic Wolbachia bacteria that infect the filarial nematode Onchocerca volvulus were previously fo

181 localization of a related cathepsin L in the filarial nematode Onchocerca volvulus, eggshell and cuti

182 iator of corneal inflammation induced by the filarial nematode Onchocerca volvulus, which harbors end

183 Filarial nematode parasites establish long-term chronic

184 ly infected with Litomosoides sigmodontis, a filarial nematode, and Schistosoma mansoni, a blood fluk

185 nt with this, we have previously described a filarial nematode-derived, secreted phosphorylcholine-co

186 Litomosoides sigmodontis, a tissue-invasive filarial nematode.

187 moproteus and Plasmodium spp.) and parasitic filarial nematodes (microfilariae) in wild birds (New Ca

188 ed for C. elegans as well those found in the filarial nematodes Acanthocheilonema viteae, Onchocerca

189 Parasitic filarial nematodes are often tolerated in human hosts fo

190 Wolbachia endosymbionts of filarial nematodes are vital for larval development and

191 or human diseases caused by the insect-borne filarial nematodes Brugia, Wuchereria and Loa.

192 We present here a review of the primary filarial nematodes causing human infection, including an

193 Symbiotic Wolbachia organisms of filarial nematodes have received much attention as possi

194 hat its presence inhibits the development of filarial nematodes in the mosquito.

195 Parasitic filarial nematodes infect more than 200 million individu

196 Filarial nematodes persist in the parasitized host by mo

197 lso targeting drug to the lymph nodes, where filarial nematodes reside in infected patients, leading

198 th substantial curative activity against the filarial nematodes responsible for LF (Brugia malayi, Wu

199 rifampicin deplete essential Wolbachia from filarial nematodes that cause lymphatic filariasis or on

200 iotic Wolbachia bacteria are abundant in the filarial nematodes that cause onchocerciasis (river blin

201 The filarial nematodes that cause these diseases are transmi

202 river blindness in which soluble extracts of filarial nematodes were injected into the corneal stroma

203 cluding dengue virus (DENV), Plasmodium, and filarial nematodes, but the molecular mechanism involved

204 thropod symbiont Wolbachia and occur in many filarial nematodes, including Brugia pahangi and Brugia

205 in the pathophysiology of diseases caused by filarial nematodes, including lymphatic filariasis and o

206 ns in Africa and South America caused by the filarial nematodes, Mansonella perstans, M. ozzardi, M.

207 Wolbachia, symbiotic bacteria living within filarial nematodes, may be involved in disease progressi

208 Filarial nematodes, parasites of vertebrates, including

209 Filarial nematodes, parasitic worms that cause elephanti

210 tion from the mammal-dominated host range of filarial nematodes, we hypothesize that these major huma

211 In filarial nematodes, which host a mutualistic association

212 efficient vector of certain arboviruses and filarial nematodes.

213 nt intracellular symbionts of arthropods and filarial nematodes.

214 a found in somatic tissues of Drosophila and filarial nematodes.

215 cies as well as some mites, crustaceans, and filarial nematodes.

216 ety of arthropods (including Drosophila) and filarial nematodes.

217 worms), or Wolbachia organisms isolated from filarial nematodes.

218 arks of patent infection with lymph-dwelling filarial nematodes.

219 searchers reported intracellular bacteria in filarial nematodes.

220 been used as highly sensitive biomarkers for filarial nematodes.

221 r endosymbiont infecting many arthropods and filarial nematodes.

222 and invasion times suggest that HTs involved filarial nematodes.

223 s), and antibiotic elimination of infectious filarial nematodes.

224 en 5a was found with sera from patients with filarial or intestinal nematode infections.

225 reover, using multiparameter flow cytometry, filarial parasite Ag induced a marked increase in not on

226 imately 90 megabase (Mb) genome of the human filarial parasite Brugia malayi and predict approximatel

227 We show that soluble extracts of the human filarial parasite Brugia malayi can induce potent inflam

228 The human filarial parasite Brugia malayi harbors an endosymbiotic

229 ility to synthesize heme; however, the human filarial parasite Brugia malayi has acquired a bacterial

230 ith soluble microfilarial Ag (MfAg) from the filarial parasite Brugia malayi in the presence of APCs.

231 termination system while others, such as the filarial parasite Brugia malayi, have an XY mechanism.

232 on methods have been developed for the human filarial parasite Brugia malayi.

233 date, giving a glimpse into the evolution of filarial parasite chromosomes and proteomes.

234 y a nutritional role of the symbiont for the filarial parasite host.

235 teraction of the host immune system with the filarial parasite is double edged, with both host protec

236 ans may play a key role in the regulation of filarial parasite numbers.

237 ective, third-stage (L3) larvae of the human filarial parasite Onchocerca volvulus, belongs to the fa

238 -Mb genome of L. loa and that of the related filarial parasite Wuchereria bancrofti and predict 14,90

239 y comparing these genomes to that of another filarial parasite, Brugia malayi, and to those of severa

240 ses was studied in a nematode model with the filarial parasite, Brugia malayi.

241 may be a strategy for immune evasion by the filarial parasite.

242 Filarial parasites are responsible for several serious h

243 Filarial parasites are tissue-dwelling nematodes respons

244 Most filarial parasites in the subfamilies Onchocercinae and

245 K cell-parasite interaction is complex, with filarial parasites inducing NK cell activation and cytok

246 flammatory response to the invasive stage of filarial parasites may be a strategy for immune evasion

247 e definitive (mammalian) host, the lymphatic filarial parasites reside in the lymph nodes and lymphat

248 vitamin B2 supplementation partially rescues filarial parasites treated with doxycycline, indicating

249 Wolbachia bacteria found in the majority of filarial parasites, failed to induce any inflammatory re

250 of loiasis overlap with those of other human filarial parasites, presenting challenges in the specifi

251 ed to be immunosuppressive when derived from filarial parasites, we determined whether R36A lacking P

252 important biochemical processes essential to filarial parasites.

253 le in down-regulating the immune response to filarial parasites.

254 zation become productively infected with the filarial parasites.

255 s known concerning promoter structure in the filarial parasites.

256 hat human CaGC has biologic activity against filarial parasites.

257 ards host cues when exposed to Brugia malayi filarial parasites.

258 phorylcholine-ES) are also released by human filarial parasites; hence we discuss how these findings

259 Disease infectivity initiates from the filarial parasitic nematode Onchocerca volvulus, which i

260 Loa loa, the African eyeworm, is a major filarial pathogen of humans.

261 hereria bancrofti (WbGST), a major lymphatic filarial pathogen of humans.

262 me PCR assays for the four most common human filarial pathogens among blood and tissue samples collec

263 This includes filarial pathogens such as Onchocerca volvulus, the caus

264 sence of infection or infection with related filarial pathogens.

265 ertainties and gaps in data and knowledge of filarial population dynamics and the effectiveness of cu

266 of alternative activation and that secreted filarial products skew monocytes similarly.

267 tyrosine kinase inhibitors bind and inhibit filarial protein activity.

268 The acylation of filarial proteins with fluorescent probes or biotin was

269 y mediator of this process is yet unknown in filarial research.

270 amma responses, and contrasted with those of filarial-sensitized newborns, who had sustained and elev

271 A novel filarial serine protease inhibitor (SPI) from the human

272 s, which we then map to the genomes of other filarial species and more distantly related nematodes.

273 Most filarial species that infect people co-exist in mutualis

274 m) and 6 pan-Phylum Nematoda (intestinal and filarial species) small molecule inhibitors were identif

275 amplify non-target DNAs from closely related filarial species, human or vectors.

276 nce or sensitization affect the evolution of filarial-specific immunity and susceptibility to W. banc

277 We tested the hypothesis that filarial-specific T cell responses at birth that are ind

278 a deficit in preclinical research tools for filarial translational research by developing Loa loa mo

279 n information using generalized knowledge of filarial transmission dynamics, monitoring survey data,

280 icrofilaremic filarial-infected (Inf) and 14 filarial-uninfected (Uninf) subjects following stimulati

281 odies were measured in filarial-infected and filarial-uninfected patients.

282 In comparison with filarial-uninfected subjects, filarial infection was ass

283 erminal domain of a metalloprotease from the filarial worm Brugia malayi.

284 ema viteae has been evaluated as a surrogate filarial worm for studying immunity to the infection.

285 y, we identify that control of chronic adult filarial worm infection is evident in IL-4Ralpha-deficie

286 t into the protective immune response to the filarial worm Onchocerca volvulus in humans.

287 rstand the role of chemosensory signaling in filarial worm taxis, we employ comparative genomics, tra

288 primary vector of West Nile virus (WNV), the filarial worm Wuchereria bancrofti, and an avian malaria

289 cation of chemosensory signaling proteins in filarial worms and encourage a more thorough investigati

290 Genomic studies of filarial worms can improve our understanding of their bi

291 st) stages in nematode life cycles, and that filarial worms contain compact and highly diverged chemo

292 e treatment modalities do not kill the adult filarial worms effectively; hence, there is a need to id

293 effective in reducing the Wolbachia load in filarial worms following oral administration to mice.

294 Infection with filarial worms significantly reduced flight distance but

295 The invasion and migration of filarial worms through host tissues are complex and crit

296 pathogen interactions involving arboviruses, filarial worms, bacteria, and malaria parasites, reveali

297 other human pathogens including viruses and filarial worms, but have never been observed to transmit

298 roteins and perturb chemotaxis phenotypes in filarial worms.

299 important in understanding disease caused by filarial worms.

300 inhibitors against Wolbachia endobacteria of filarial worms.