ライフサイエンスコーパス: filarial

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

2 BMC supernatants generated from MF patients, filarial Ag (Brugia malayi adult Ag (BmA))-stimulated su

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 These data demonstrate that filarial Ags by themselves can specifically prime CD45RA

10 Schistosome and filarial Ags stimulated a 3- to > 100-fold increase in t

11 RA+ CD4+ cells, demonstrating the ability of filarial Ags to prime naive T cells in the absence of ex

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

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

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

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

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

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

18 The absence of circulating filarial antigen was associated with Th1-like responses,

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

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

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

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

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

24 The relationship between filarial antigenemia and lymphatic pathology was investi

25 determined by blood-borne microfilariae and filarial antigenemia.

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

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

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

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

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

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

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

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

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

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

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

37 uals produced IL-5 mRNA in response to adult filarial antigens, and total parasite-specific IL-4 and

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

39 ated with systemic inflammatory reactions to filarial chemotherapy.

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

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

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

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

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

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

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

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

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

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

50 a narrower spectrum would aid in eliminating filarial diseases.

51 0.4% (P=0.005), and the rate of detection of filarial DNA decreased from 19.4% to 14.9% (P=0.13).

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

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

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

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

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

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

58 Wolbachia containing filarial extracts stimulated cytokine production in macr

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

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

61 culated with S. mansoni ova, larvae from the filarial helminth Brugia malayi, or CFA.

62 Human filarial helminth infections are characterized by type 2

63 ils are required for the induction of AHR by filarial helminths.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

83 Filarial infection is initiated by mosquito-derived thir

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

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

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

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

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

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

90 Filarial infection was also associated with a marked inc

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

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

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

94 Importantly, filarial infection was associated with markedly lower fr

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

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

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

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

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

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

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

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

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

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

105 cific T cell unresponsiveness seen in patent filarial infection.

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

107 l hyporesponsiveness in patients with patent filarial infection.

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

109 ay promote the posttreatment eosinophilia in filarial infection.

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

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

112 The diagnosis of filarial infections among individuals residing in areas

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

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

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

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

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

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

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

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

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

122 Filarial infections evoke exuberant inflammatory respons

123 Filarial infections have been associated with the develo

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

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

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

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

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

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

130 Filarial infections of humans cause some of the most imp

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

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

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

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

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

136 patients undergoing evaluation for suspected filarial infections.

137 7 CD4(+) cells are expanded in vivo in human filarial infections.

138 important role in determining the outcome of filarial infections.

139 responsible for most immune dysregulation in filarial infections.

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

141 is a quintessential feature of chronic human filarial infections.

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

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

144 genesis of lymphatic lesions associated with filarial infections.

145 rophils and involved in host defense against filarial infections.

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

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

148 lation through endothelium and into sites of filarial inflammation was investigated in asymptomatic m

149 Thus, IL-4 produced in vivo in response to filarial L3 and adult parasites is essential for the ind

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

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

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

153 Recently developed filarial molecular diagnostic assays are highly sensitiv

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

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

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

157 62, a glycoprotein secreted by the parasitic filarial nematode Acanthocheilonema viteae, subverts hos

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

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

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

161 Heme acquisition in the parasitic filarial nematode Brugia malayi.

162 hsp83 was cloned from the filarial nematode Brugia pahangi.

163 or mediators of inflammatory pathogenesis in filarial nematode disease.

164 The filarial nematode gene Bmgmf for Brugia malayi glia matu

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

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

167 evolved as essential endosymbionts of their filarial nematode hosts.

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

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

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

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

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

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

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

175 The filarial nematode Onchocerca volvulus is the causative o

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

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

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

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

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

181 Filarial nematode parasites establish long-term chronic

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

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

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

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

186 Parasitic filarial nematodes are often tolerated in human hosts fo

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

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

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

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

191 Parasitic filarial nematodes infect more than 200 million individu

192 Filarial nematodes persist in the parasitized host by mo

193 Filarial nematodes require both an arthropod vector and

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

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

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

197 The filarial nematodes that cause these diseases are transmi

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

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

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

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

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

203 Filarial nematodes, parasites of vertebrates, including

204 Filarial nematodes, parasitic worms that cause elephanti

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

206 In filarial nematodes, which host a mutualistic association

207 r endosymbiont infecting many arthropods and filarial nematodes.

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

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

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

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

212 searchers reported intracellular bacteria in filarial nematodes.

213 and invasion times suggest that HTs involved filarial nematodes.

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

215 actions during the growth and development of filarial nematodes.

216 efficient vector of certain arboviruses and filarial nematodes.

217 nt intracellular symbionts of arthropods and filarial nematodes.

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

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

220 ntaining glycoprotein released by the rodent filarial parasite Acanthocheilonema viteae, interferes w

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

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

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

224 The human filarial parasite Brugia malayi harbors an endosymbiotic

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

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

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

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

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

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

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

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

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

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

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

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

237 Filarial parasites are responsible for several serious h

238 Filarial parasites are tissue-dwelling nematodes respons

239 Most filarial parasites in the subfamilies Onchocercinae and

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

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

242 Here we report that filarial parasites of humans secrete a homologue of the

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

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

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

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

247 sopeptide bonds in the sheath and cuticle of filarial parasites, suggesting an important role for TGa

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

249 important biochemical processes essential to filarial parasites.

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

251 zation become productively infected with the filarial parasites.

252 s known concerning promoter structure in the filarial parasites.

253 hat human CaGC has biologic activity against filarial parasites.

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

255 cuticle during the growth and maturation of filarial parasites.

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

257 GF-beta) receptor has been isolated from the filarial parasitic nematode Brugia pahangi.

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

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

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

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

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

263 sence of infection or infection with related filarial pathogens.

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

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

266 tyrosine kinase inhibitors bind and inhibit filarial protein activity.

267 Using two recombinant filarial protein Ags and keyhole limpet hemocyanin, we s

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

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

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

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

272 re also found to be expressed in the related filarial species Wuchereria bancrofti and Onchocerca vol

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

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

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

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

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

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

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

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

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

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

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

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

285 important in understanding disease caused by filarial worms.

286 is up-regulated when A. aegypti encapsulates filarial worms.

287 inhibitors against Wolbachia endobacteria of filarial worms.