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1 nt mice displayed enhanced susceptibility to Yersinia infection.
2 to gain insight into the initial stages of a Yersinia infection.
3 ue and other pathogenic conditions caused by Yersinia infection.
4 e cells, and were attenuated in disseminated Yersinia infection.
5 nt to support a detectable increased risk of Yersinia infection.
6 flammatory circuit that restricts intestinal Yersinia infection.
7 ent mice showed heightened susceptibility to Yersinia infection.
8  for bacterial containment following enteric Yersinia infection.
9  to enable PG-mediated control of intestinal Yersinia infection.
10 tures termed pyogranulomas (PG) that control Yersinia infection.
11  important for virulence in murine models of Yersinia infection.
12 novel, antivirulence strategy for preventing Yersinia infection.
13 c colonization in mouse models of intestinal Yersinia infection.
14 ) and TLR2(-/-) mice during enteropathogenic Yersinia infection.
15  vivo cell death-dependent immune control of Yersinia infection, a physiological model of TAK1/IKK in
16 ene expression in macrophages in response to Yersinia infection and that YopJ deactivates both pathwa
17 he processing of MyD88 was not restricted to Yersinia infection and to proapoptotic Toll-IL-1R domain
18        Mice lacking T cells are sensitive to Yersinia infection, and a humoral response to Yersinia c
19                   Unless the pathogenesis of Yersinia infection differs markedly between mice and hum
20                               In response to Yersinia infection, FADD, RIPK1 and caspase-8 were recru
21  YopR are essential for the establishment of Yersinia infections in a mouse model system, suggesting
22                                Nevertheless, Yersinia infection induces inflammatory responses in viv
23 th digitonin to measure Yop targeting during Yersinia infections of HeLa cells.
24                  Successful establishment of Yersinia infections requires the type III machinery, a p
25 y in the HeLa cell nucleus after delivery by Yersinia infection, showing that these LRRs are not esse
26 e expression profile of gammadelta IELs in a Yersinia infection system to better define their roles.
27  TGF-beta+ T-regulatory cells (T-regs) after Yersinia infection that is reduced in ovalbumin T-cell r
28 ction, we postulate that a silent persistent Yersinia infection was reactivated, leading to dissemina
29 ression and targeting of Yop proteins during Yersinia infection, whereas secreted LcrV is required to