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1 most patients with systemic sarcoidosis have hepatic granulomas, a minority will experience significa
2                                              Hepatic granulomas also contained large numbers of dying
3           The incidence of cell death within hepatic granulomas also decreased significantly in the a
4 strate significant frequencies of naTregs in hepatic granulomas and draining lymphoid tissues of mice
5 ed IL-4Ralpha KO mice developed only minimal hepatic granulomas and fibrosis despite the presence of
6 eficient mice did not form normal numbers of hepatic granulomas and showed widely disseminated Franci
7 a mansoni- and Schistosoma japonicum-induced hepatic granuloma are also discussed.
8 e helminth Schistosoma mansoni develop small hepatic granulomas around parasite eggs, but concomitant
9 stosome eggs may promote angiogenesis within hepatic granulomas by up-regulating endothelial cell VEG
10                                              Hepatic granuloma cells from egg-tolerized mice were als
11 r accounting for the absence of IFN-gamma in hepatic granuloma cultures.
12  an in silico Petri net model that simulates hepatic granuloma development throughout the course of i
13 r, both IKKalpha and IKKbeta have effects on hepatic granuloma development.
14 onovani infected BALB/c mice, IL-13 promotes hepatic granuloma formation and controls parasite burden
15                   In this study, we analyzed hepatic granuloma formation and egg-induced cytokine pro
16 , we have asked what role IFN-gamma plays in hepatic granuloma formation and function.
17 f endogenous IL-10 in the down-modulation of hepatic granuloma formation and lymphocyte responses tha
18 lition of the development of the SCW-induced hepatic granuloma formation and matrix expansion.
19           However, significant inhibition of hepatic granuloma formation associated with the natural
20 sts that TGF-beta 1 gene transfer suppresses hepatic granuloma formation by blocking the recruitment
21       In infection with Schistosoma mansoni, hepatic granuloma formation is mediated by CD4(+) T help
22                                    Defective hepatic granuloma formation was not corrected by transfe
23 during F. tularensis LVS infections regulate hepatic granuloma formation, the spatial containment of
24 e loads than WT controls and showed impaired hepatic granuloma formation.
25  Schistosomiasis mansoni is characterized by hepatic granuloma formation.
26 mune priming by these Ag(s) is necessary for hepatic granuloma formation.
27                                              Hepatic granulomas in Stat6-deficient mice were composed
28 yed significantly more developing and mature hepatic granulomas leading to reduction in organ parasit
29                                Moreover, the hepatic granuloma lymphocytes at 6.5 wk responded to p38
30 rea and in the peripheral blood, spleen, and hepatic granulomas of S. mansoni-infected high-pathology
31        When mature eosinophils isolated from hepatic granulomas of Schistosoma mansoni-infected mice
32 d the role of IL-33 and its receptor ST2L in hepatic granuloma pathology induced by Schistosoma japon
33 e data demonstrate that IL-33 contributes to hepatic granuloma pathology through induction of M2 macr
34  and oviposition rates and small (modulated) hepatic granulomas showed the opposite pattern: HPA axis
35 10T mice displayed a significant increase in hepatic granuloma size at the acute stage of infection,
36 oupled with the development of pulmonary and hepatic granulomas that were greatly decreased in size c
37 of effector cytokines by CD4+ T cells within hepatic granulomas triggered by Bacille Calmette-Guerin
38  for ICAM-1 in recruiting lymphocytes to the hepatic granuloma was also supported by the observation
39  cells were recruited to the spleen and into hepatic granulomas, where they inhibited host protective
40 asites coupled with ill-defined and immature hepatic granulomas, whereas in WT mice there were less o