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1 ficient T cells are defective in controlling Listeria infection.
2 knowledge on the Vip-Gp96 interaction during Listeria infection.
3 n be activated and confer protection against Listeria infection.
4 ophils to the decidual tissue in response to Listeria infection.
5 duced CD8(+) T cell response to a subsequent 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 hagocytic cells is dramatically induced upon Listeria infection.
14 nflammatory cytokines during endotoxemia and Listeria infections.
15 okine responses during primary and secondary Listeria infections.
16 critical roles in the survival of DCs during Listeria infection, allowing DCs to function in innate a
17 ver, mice lacking TNFR1 in MDCs succumbed to listeria infection, although they displayed similar sens
18 -specific CD8 T cells at different stages of Listeria infection and analyzed the effect of deletion o
19 hils are an early source of IFN-gamma during Listeria infection and are important in providing immune
20 ability of CD8(+) T cells to protect against Listeria infection and attenuate tumor growth in vivo.
21 ) T cells were more effective at controlling Listeria infection and B16 melanoma growth in vivo, and
22 C/SLEC differentiation choice following both Listeria infection and dendritic cell immunization of mi
23 d in both primary and secondary responses to Listeria infection and developed even when infection was
24 ce showed reduced efficiency in clearance of Listeria infection and exert a protective effect against
25 rferon (IFN) receptor were more resistant to Listeria infection and had less apoptotic lesions than w
26 d IFN-gamma secretion by CD8+ T cells during Listeria infection and that care must be taken when inte
27 is also a major player in the resolution of Listeria infections and is suggested to have more global
28 These T cells are protective against primary Listeria infection, as Listeria-infected K(b-/-)D (b-/-)
29 effector CD8(+) T cell differentiation upon listeria infection but did result in a severe defect in
33 s protects recipient mice against subsequent Listeria infection in a CD8(+) T cell-dependent manner.
39 the influence of physiological stressors and Listeria infection on host Hsp60 expression and LAP-medi
40 bsent from fragmented mitochondria following Listeria infection or LLO treatment, as the dynamin-like
43 characterized ISG15-dependent restriction of Listeria infection, reinforcing the view that ISG15 is a
44 because BALB/c mice are more susceptible to Listeria infection than other commonly studied mouse str
45 appears to be an obligatory step in primary Listeria infection, the extent of which is controlled by
47 llenge with Listeria, the overall control of Listeria infection was impaired in Flt3-L-treated mice,
49 susceptible than wild-type mice to systemic Listeria infection, which correlates with increased numb
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