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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.

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