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1 malaria (Plasmodium chabaudi) and nematodes (Nippostrongylus brasiliensis).
2 dwelling nematodes (Trichinella spiralis and Nippostrongylus brasiliensis).
3 tinal helminths Heligmosomoides polygyrus or Nippostrongylus brasiliensis.
4 in vivo and contributed to the expulsion of Nippostrongylus brasiliensis.
5 ctions following infection with the helminth Nippostrongylus brasiliensis.
6 n with the phylogenetically distant nematode Nippostrongylus brasiliensis.
7 ce to the natural murine parasitic nematode, Nippostrongylus brasiliensis.
8 nfections with Heligmosomoides polygyrus and Nippostrongylus brasiliensis.
9 mnestic immunity against the rodent hookworm Nippostrongylus brasiliensis.
10 protease allergen, as well as infection with Nippostrongylus brasiliensis.
11 ytokine in the early type 2 immunity against Nippostrongylus brasiliensis.
12 red Th2 cell development upon infection with Nippostrongylus brasiliensis.
13 n of mice with the gastrointestinal helminth Nippostrongylus brasiliensis.
14 nt hapten-protein conjugate and the helminth Nippostrongylus brasiliensis.
15 ype 2 immunity against the hookworm parasite Nippostrongylus brasiliensis.
16 ice with Heligmosomoides polygyrus bakeri or Nippostrongylus brasiliensis.
17 ource of IL13 during helminth infection with Nippostrongylus brasiliensis.
18 soma mansoni and much more susceptibility to Nippostrongylus brasiliensis.
19 were inoculated with the nematode parasite, Nippostrongylus brasiliensis.
20 cted with the migrating intestinal helminth, Nippostrongylus brasiliensis.
21 response elicited by helminth infection with Nippostrongylus brasiliensis.
22 -gamma-producing cells in mice infected with Nippostrongylus brasiliensis.
23 uring infection with the intestinal nematode Nippostrongylus brasiliensis.
24 esterase (AChE B) from the nematode parasite Nippostrongylus brasiliensis.
25 d during the host response to infection with Nippostrongylus brasiliensis.
26 after infection with the helminthic parasite Nippostrongylus brasiliensis.
27 parasites, such as Tritrichomonas muris and Nippostrongylus brasiliensis.
28 plasia following infection with the helminth Nippostrongylus brasiliensis.
29 assist in the increasing clearance of adult Nippostrongylus brasiliensis, a gastrointestinal nematod
31 on of both proteins following infection with Nippostrongylus brasiliensis, a hookworm that infects th
33 cytokines was produced during infection with Nippostrongylus brasiliensis, a Th2-inducing stimulus, a
34 Unexpectedly, challenge of these mice with Nippostrongylus brasiliensis, a Th2-inducing stimulus, f
35 sion of VAT eosinophils after infection with Nippostrongylus brasiliensis, an intestinal parasite ass
36 terize CX3CR1+CD4+ T cells during both acute Nippostrongylus brasiliensis and chronic Schistosoma man
37 2-inducing pathogens Schistosoma mansoni and Nippostrongylus brasiliensis and examined the influence
38 lung injury caused by the hookworm parasite Nippostrongylus brasiliensis and for type 2 immunity aft
39 chitin-containing gastrointestinal nematodes Nippostrongylus brasiliensis and Heligmosomoides polygyr
40 eous expulsion and IL-4-induced expulsion of Nippostrongylus brasiliensis and Heligmosomoides polygyr
41 d their responsiveness during infection with Nippostrongylus brasiliensis and protease allergen-induc
44 of two gastrointestinal nematode parasites, Nippostrongylus brasiliensis and Trichinella spiralis, i
45 controlled infection with Leishmania major, Nippostrongylus brasiliensis, and Theiler's murine encep
46 IL-33 and after infection with the helminth Nippostrongylus brasiliensis, and they are the major inn
47 nt gastrointestinal nematodes (H. polygyrus, Nippostrongylus brasiliensis, and Trichinella spiralis)
48 o tissues of mice infected with the helminth Nippostrongylus brasiliensis, but eosinophils failed to
49 and host resistance to the hookworm parasite Nippostrongylus brasiliensis Collectively, these data un
50 C57BL/6 mice fed a high-fat diet (HFD) with Nippostrongylus brasiliensis decreased weight gain and w
51 with the gastrointestinal nematode parasite Nippostrongylus brasiliensis demonstrated that IL-4/IL-1
52 t-killed Brucella abortus, or infection with Nippostrongylus brasiliensis demonstrates selectively im
54 n of the gastrointestinal nematode parasite, Nippostrongylus brasiliensis, from immunodeficient mice,
55 efense against the gastrointestinal nematode Nippostrongylus brasiliensis; however, the role of IL-13
57 nfection with the soil-transmitted hookworm, Nippostrongylus brasiliensis, in its early host intrapul
58 on, and diminished eosinophilic responses to Nippostrongylus brasiliensis, increasing parasite burden
60 shed that infection with the rodent hookworm Nippostrongylus brasiliensis induces a strongly polarize
63 o animal models of type 2 lung inflammation, Nippostrongylus brasiliensis infection and house dust mi
65 investigated the regulation of IL-25 during Nippostrongylus brasiliensis infection and the contribut
66 se to DNP-keyhole limpet hemocyanin/alum and Nippostrongylus brasiliensis infection compared with tha
67 o analysis of peritoneal inflammation during Nippostrongylus brasiliensis infection in mice revealed
69 ooth muscle contractility, 2) the effects of Nippostrongylus brasiliensis infection on PAR-1 response
70 nhibited tuft cell responses to heterologous Nippostrongylus brasiliensis infection or succinate, and
72 models of immunization, allergic asthma, and Nippostrongylus brasiliensis infection, likely by induci
74 s to bypass the lung or intestinal phases of Nippostrongylus brasiliensis infection, we show that blo
77 The host defence against helminths such as Nippostrongylus brasiliensis is orchestrated by type 2 c
78 larvae from the helminth parasite nonviable Nippostrongylus brasiliensis L3 larvae (Nb), a strong in
80 different Th2 stimuli: the helminth parasite Nippostrongylus brasiliensis (Nb) and the contact sensit
81 h nodes (MLNs) and lung after infection with Nippostrongylus brasiliensis (Nb) as a human hookworm in
82 t mice infected with the intestinal helminth Nippostrongylus brasiliensis (Nb) exhibit a transitory i
83 have now examined the Th2 immune response to Nippostrongylus brasiliensis (Nb) in B7-1/B7-2(-/-) mice
85 immunomodulation, with increased survival of Nippostrongylus brasiliensis (Nb)-infected hRETNTg(+) mi
87 e, we show that an acute helminth infection (Nippostrongylus brasiliensis [Nb]) induced a type 2 immu
88 xpel the parasitic gastrointestinal nematode Nippostrongylus brasiliensis normally [4], suggesting th
89 , B cell-deficient mice were inoculated with Nippostrongylus brasiliensis or Heligmosomoides polygyru
90 d expulsion of the gastrointestinal nematode Nippostrongylus brasiliensis or induction of lung inflam
92 ate groups of BALB/c mice were infected with Nippostrongylus brasiliensis or were drug-cured of an in
93 histosoma mansoni, intestinal infection with Nippostrongylus brasiliensis, or induction of airway hyp
94 infection with the gastrointestinal helminth Nippostrongylus brasiliensis Our results identify a nove
96 infection with the lung-migrating nematode, Nippostrongylus brasiliensis, suggesting a potential rol
97 ed ability to expulse the helminth parasite, Nippostrongylus brasiliensis These results prompt the qu
98 g suppression is suggested by the ability of Nippostrongylus brasiliensis to elicit hyporesponsivenes
99 L-25 and IL-33 or infected with the helminth Nippostrongylus brasiliensis to induce innate type 2 all
101 g a rodent model of infection with hookworm (Nippostrongylus brasiliensis), we characterized the long
102 tes, including Heligmosomoides polygyrus and Nippostrongylus brasiliensis, we first confirmed the req
104 uring infection with the parasitic nematode, Nippostrongylus brasiliensis, which is known to induce e
105 LC2s during the lung stage of infection with Nippostrongylus brasiliensis, which results in substanti