ライフサイエンスコーパス: hepatic granuloma

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1 Hepatic granulomas also contained large numbers of dying

2 The incidence of cell death within hepatic granulomas also decreased significantly in the a

3 strate significant frequencies of naTregs in hepatic granulomas and draining lymphoid tissues of mice

4 ed IL-4Ralpha KO mice developed only minimal hepatic granulomas and fibrosis despite the presence of

5 eficient mice did not form normal numbers of hepatic granulomas and showed widely disseminated Franci

6 a mansoni- and Schistosoma japonicum-induced hepatic granuloma are also discussed.

7 e helminth Schistosoma mansoni develop small hepatic granulomas around parasite eggs, but concomitant

8 stosome eggs may promote angiogenesis within hepatic granulomas by up-regulating endothelial cell VEG

9 Hepatic granuloma cells from egg-tolerized mice were als

10 r accounting for the absence of IFN-gamma in hepatic granuloma cultures.

11 an in silico Petri net model that simulates hepatic granuloma development throughout the course of i

12 r, both IKKalpha and IKKbeta have effects on hepatic granuloma development.

13 onovani infected BALB/c mice, IL-13 promotes hepatic granuloma formation and controls parasite burden

14 In this study, we analyzed hepatic granuloma formation and egg-induced cytokine pro

15 , we have asked what role IFN-gamma plays in hepatic granuloma formation and function.

16 f endogenous IL-10 in the down-modulation of hepatic granuloma formation and lymphocyte responses tha

17 lition of the development of the SCW-induced hepatic granuloma formation and matrix expansion.

18 However, significant inhibition of hepatic granuloma formation associated with the natural

19 sts that TGF-beta 1 gene transfer suppresses hepatic granuloma formation by blocking the recruitment

20 In infection with Schistosoma mansoni, hepatic granuloma formation is mediated by CD4(+) T help

21 Defective hepatic granuloma formation was not corrected by transfe

22 during F. tularensis LVS infections regulate hepatic granuloma formation, the spatial containment of

23 Schistosomiasis mansoni is characterized by hepatic granuloma formation.

24 mune priming by these Ag(s) is necessary for hepatic granuloma formation.

25 Hepatic granulomas in Stat6-deficient mice were composed

26 Moreover, the hepatic granuloma lymphocytes at 6.5 wk responded to p38

27 rea and in the peripheral blood, spleen, and hepatic granulomas of S. mansoni-infected high-pathology

28 When mature eosinophils isolated from hepatic granulomas of Schistosoma mansoni-infected mice

29 d the role of IL-33 and its receptor ST2L in hepatic granuloma pathology induced by Schistosoma japon

30 e data demonstrate that IL-33 contributes to hepatic granuloma pathology through induction of M2 macr

31 and oviposition rates and small (modulated) hepatic granulomas showed the opposite pattern: HPA axis

32 10T mice displayed a significant increase in hepatic granuloma size at the acute stage of infection,

33 oupled with the development of pulmonary and hepatic granulomas that were greatly decreased in size c

34 of effector cytokines by CD4+ T cells within hepatic granulomas triggered by Bacille Calmette-Guerin

35 for ICAM-1 in recruiting lymphocytes to the hepatic granuloma was also supported by the observation

36 cells were recruited to the spleen and into hepatic granulomas, where they inhibited host protective

37 asites coupled with ill-defined and immature hepatic granulomas, whereas in WT mice there were less o

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