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1 duced CD8(+) T cell response to a subsequent Listeria infection.
2 hagocytic cells is dramatically induced upon Listeria infection.
3 knowledge on the Vip-Gp96 interaction during Listeria infection.
4 n be activated and confer protection against Listeria infection.
5 ophils to the decidual tissue in response to Listeria infection.
6 edominance of triple-positive cells required Listeria infection.
7 han those in TRAIL-/- mice following primary Listeria infection.
8 nctional memory CD8 T cell populations after Listeria infection.
9 mice more susceptible than CapG(+/+) mice to Listeria infection.
10 of Ag-specific CD4 and CD8 T cells following Listeria infection.
11 to secrete both TNF and nitric oxide after a Listeria infection.
12  oxidase showed heightened susceptibility to Listeria infection.
13 ent TVM cells failed to protect mice against Listeria infection.
14 e metabolism of CD8(+) T cells responding to Listeria infection.
15 ficient T cells are defective in controlling Listeria infection.
16 nflammatory cytokines during endotoxemia and Listeria infections.
17 s demonstrate a crucial role for CypA during Listeria infections.
18 okine responses during primary and secondary Listeria infections.
19                                              Listeria infection activated the RIPK3-MLKL pathway in c
20 critical roles in the survival of DCs during Listeria infection, allowing DCs to function in innate a
21 ver, mice lacking TNFR1 in MDCs succumbed to listeria infection, although they displayed similar sens
22 -specific CD8 T cells at different stages of Listeria infection and analyzed the effect of deletion o
23 hils are an early source of IFN-gamma during Listeria infection and are important in providing immune
24 ability of CD8(+) T cells to protect against Listeria infection and attenuate tumor growth in vivo.
25 ) T cells were more effective at controlling Listeria infection and B16 melanoma growth in vivo, and
26 crophages, and cDC1s in the MZ promotes both Listeria infection and CD8(+) T cell activation.
27 C/SLEC differentiation choice following both Listeria infection and dendritic cell immunization of mi
28 d in both primary and secondary responses to Listeria infection and developed even when infection was
29 ce showed reduced efficiency in clearance of Listeria infection and exert a protective effect against
30 rferon (IFN) receptor were more resistant to Listeria infection and had less apoptotic lesions than w
31 d IFN-gamma secretion by CD8+ T cells during Listeria infection and that care must be taken when inte
32  is also a major player in the resolution of Listeria infections and is suggested to have more global
33 ll responses to dendritic cell immunization, Listeria infection, and viral infection.
34 These T cells are protective against primary Listeria infection, as Listeria-infected K(b-/-)D (b-/-)
35  effector CD8(+) T cell differentiation upon listeria infection but did result in a severe defect in
36         Histopathology showed that following Listeria infection, CD18-ko mice had milder inflammatory
37                               Upon secondary Listeria infection, CD40-/- memory CD8 T cells expand to
38                                              Listeria infection during pregnancy can cause the death
39 s protects recipient mice against subsequent Listeria infection in a CD8(+) T cell-dependent manner.
40 ouse tmTNF nor suppressed innate immunity to Listeria infection in mice.
41  we observed that ISG15 expression restricts Listeria infection in vitro and in vivo.
42 T cells in vitro was not recapitulated after Listeria infection in vivo.
43 llular replication of Listeria Surprisingly, Listeria infection-induced phosphorylation of MLKL did n
44 se role for the LAP-Hsp60 interaction during Listeria infection is unknown.
45                                       During Listeria infection, LAT(G135D) T cells expand more than
46  exacerbate systemic infection in the murine Listeria infection model.
47 the influence of physiological stressors and Listeria infection on host Hsp60 expression and LAP-medi
48 bsent from fragmented mitochondria following Listeria infection or LLO treatment, as the dynamin-like
49                              We found, after Listeria infection, plasma transforming growth factor be
50                      We found that, although Listeria infections reduced expression of CCL21 in murin
51 characterized ISG15-dependent restriction of Listeria infection, reinforcing the view that ISG15 is a
52  responses, refed mice remain susceptible to Listeria infection, revealing that recovery from lymphoi
53  because BALB/c mice are more susceptible to Listeria infection than other commonly studied mouse str
54  appears to be an obligatory step in primary Listeria infection, the extent of which is controlled by
55                    For example, 5 days after Listeria infection, the spleen and liver of ACE 10/10 mi
56 llenge with Listeria, the overall control of Listeria infection was impaired in Flt3-L-treated mice,
57                              Also, following Listeria infection, we found that the expansion and diff
58  susceptible than wild-type mice to systemic Listeria infection, which correlates with increased numb
59 by pre-colonization of germ-free mice before Listeria infection with Prevotella copri, an abundant gu