ライフサイエンスコーパス: nematode infection

1 and the insect immune response to parasitic nematode infection.

2 of resident MPhis during a Th2-biased tissue nematode infection.

3 cal mediator of resistance during intestinal nematode infection.

4 abundance of a set of antioxidant genes upon nematode infection.

5 food intake to maintain energy stores during nematode infection.

6 omeostasis throughout evolution is parasitic nematode infection.

7 es and attenuation of host resistance to the nematode infection.

8 nt and differentiation of murine MMCs during nematode infection.

9 immune-effector molecule in resistance to GI nematode infection.

10 ype 1 responses and chronic gastrointestinal nematode infection.

11 ntly intraepithelial location of MMCs during nematode infection.

12 ier function of intestinal epithelium during nematode infection.

13 ng Th cell responses during gastrointestinal nematode infection.

14 /c background to investigate the response to nematode infection.

15 in resistant than in susceptible roots after nematode infection.

16 constitutively and in inductive responses to nematode infection.

17 ivated in retroviral infection but weakly in nematode infection.

18 ey to viral, bacterial, oomycete, fungal and nematode infections.

19 ng anti-Wolbachia therapies against filarial nematode infections.

20 sms contributed to MPhi proliferation during nematode infections.

21 nses limit, and in some instances eliminate, nematode infections.

22 at limit the parasite burden during filarial nematode infections.

23 ra from patients with filarial or intestinal nematode infections.

24 We investigated the effects of nematode infection against obesity and the associated me

25 ate that the protective mechanism of enteric nematode infection against TNBS-induced colitis involves

26 wed that LeMir expression is up-regulated by nematode infection and by wounding.

27 es antagonize each other's virulence in both nematode infection and in vitro biofilm models.

28 ytokine in protective immunity to intestinal nematode infection and is believed to enhance Th2 immune

29 essfully protect the host against intestinal nematode infection and suggests that IL-9 can act as a p

30 receptor mutants revealed a decrease in both nematode infection and syncytium size.

31 Strong KRP6 expression upon nematode infection and the phenotypic resemblance betwee

32 Furthermore, both nematode infection and transient expression of Gr-VAP1 i

33 mplications for approaches to the control of nematode infections and the disease that they cause.

34 t endosymbionts in the response to parasitic nematode infections, and the influence of nematode endos

35 Nematode infections are an important economic constraint

36 Gastrointestinal (GI) nematode infections are an important public health and e

37 vation of macrophages is also analyzed, with nematode infection as prototypic disease.

38 MYB83 expression increases were conducive to nematode infection because overexpression of a noncleava

39 and CRN is not only required for successful nematode infection but is also involved in the formation

40 haracteristic changes similar to those after nematode infection but was unable to restore the impaire

41 of Th2-mediated protective immunity against nematode infection by a mechanism involving CCL2 product

42 animals were continually exposed to a mixed nematode infection by grazing.

43 that IL-13Ralpha2 plays an important role in nematode infection by limiting the availability of IL-13

44 lly produced in response to gastrointestinal nematode infections fail to enhance host protection agai

45 Gastrointestinal nematode infections generally invoke a type 2 cytokine r

46 Nematode infection had no effect on isoflavonoid levels.

47 Parasitic nematode infection has both preventive and therapeutic e

48 CLE peptides and are required for successful nematode infection; however, the receptors for nematode

49 H)1 inflammation is thought to favor chronic nematode infection, IFN-gamma was neutralized in vivo, r

50 t mice exhibit impaired Th2 immunity against nematode infection, implicating IL-25 as a key component

51 13 (IL-13)-producing ILC2s and resistance to nematode infection in mice, which revealed that ILCs are

52 ponse that facilitates a prompt clearance of nematode infection in SWR/J mice may have evolved to con

53 ta0.3 TobRB7 promoter, which is induced upon nematode infection in tobacco roots.

54 ons that occur at an extraintestinal site of nematode infection in which the eosinophil functions as

55 Nematode infection induced a STAT6-dependent increase in

56 ata show that IL-25 plays a critical role in nematode infection-induced alterations in intestinal fun

57 Parasitic nematode infection induces a polarized Th2 cytokine resp

58 Enteric nematode infection induces a smooth muscle hypercontract

59 Enteric nematode infection induces a strong type 2 T helper cell

60 119 GHE disease states (excluding intestinal nematode infections, iodine deficiency, and vitamin A de

61 Gastrointestinal nematode infection is known to alter host T cell activat

62 Rapid induction of expression upon nematode infection is localized to root tips.

63 of MPhis during intestinal as well as tissue nematode infection is restricted to sites of IL-4 produc

64 ive pathogen is necessary for virulence in a nematode infection model and for efficient killing of cu

65 n silicone elastomers, and pathogenesis in a nematode infection model as well as alters fungal morpho

66 development of IL-4-expressing B cells in a nematode infection model was dependent on both T cells a

67 Analysis of a nematode infection model, in which the parasite migrates

68 rasite expulsion in several gastrointestinal nematode infection models.

69 -characterized mouse model of human filarial nematode infection, nematode survival and protective imm

70 ionship in ruminants, using gastrointestinal nematode infections of sheep as the model system.

71 akeri polygyrus to investigate the impact of nematode infections on malarial morbidity and antimalari

72 f these immune cells in host defense against nematode infection remains poorly defined.

73 he host mechanism of defense against enteric nematode infection remains to be fully understood, but i

74 -standing paradigm of eosinophil toxicity in nematode infection requires reevaluation, as our results

75 Before nematode infection, RNA blot analysis revealed 1.3-1.8-f

76 r show that StCLV2 is highly up-regulated at nematode infection sites and that transgenic potatoes wi

77 The chronic nature of intestinal nematode infections suggests that these parasites have e

78 ding the insect immune response to parasitic nematode infection that consists of seven species of EPN

79 After nematode infection, the mRNAs declined over 48 h in resi

80 Nematode infection upregulates interleukin-4 (IL-4) and

81 weight was maintained in both strains during nematode infection via different mechanisms.

82 phenotype" is advantageous during intestinal nematode infection, we compared the responses to Heligmo

83 nferred susceptibility to drought stress and nematode infection when overexpressed.

84 e are more energy efficient during parasitic nematode infection, which may explain their ability to t

85 re we show, using separate models of pleural nematode infection with Litomosoides sigmodontis and Alt

86 sociated with the establishment of parasitic nematode infections within the gastrointestinal environm

87 ion as a therapeutic agent against parasitic nematode infection worldwide.