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1  cells indicated IMD pathway activation upon rickettsial infection.
2 tress-induced toxic nucleotide levels during rickettsial infection.
3  the protective inflammatory response during rickettsial infection.
4   CTLs appear to be crucial to recovery from rickettsial infection.
5 s was not the explanation for the control of rickettsial infection.
6 and prevented the suppression of the initial rickettsial infection.
7 te production and suppression of the initial rickettsial infection.
8 ntibody-mediated killing confers immunity to rickettsial infection.
9 s of the immune response, remains unclear in rickettsial infections.
10 educe inflammatory damage to the host during rickettsial infections.
11 ole early during the immune response against rickettsial infections.
12 (a scavenger of extracellular NO) during the rickettsial infection alleviated the suppression of the
13  may also contribute to the establishment of rickettsial infection and resulting pathogenesis.
14 r interleukin-12 (IL-12) p40 production upon rickettsial infection and were more potent in priming na
15 charide exhibited suppression of the initial rickettsial infection, and the suppression was relieved
16                        Although survivors of rickettsial infections are considered immune to disease,
17 d against the major infected target cells of rickettsial infections, endothelial cells and macrophage
18 mune regulatory mechanisms involved in fatal rickettsial infection have been unknown.
19       Thus, type I IFNs are induced during a rickettsial infection in vivo and promote severe disease
20 ions may be as common as spotted fever group rickettsial infections in febrile patients from central
21 hermore, NK cells are involved in preventing rickettsial infection-induced endothelial cell damage, p
22       Human cells are capable of controlling rickettsial infections intracellularly, the most relevan
23      Delineating the molecular mechanisms of rickettsial infection is critical to a thorough understa
24 on alleviated the suppression of the initial rickettsial infection observed in appropriately treated
25 travelers returning from sub-Saharan Africa, rickettsial infection, primarily tick-borne spotted feve
26  activity was more critical to recovery from rickettsial infection than were the effects of IFN-gamma
27 , in relevant animal models that mimic human rickettsial infections, there is reciprocal immunologica
28 product of NO) were produced and the initial rickettsial infection was suppressed in cultures of L929
29                   To address if fleas combat rickettsial infection, we characterized the cat flea (Ct
30 factors associated with the tick response to rickettsial infection, we utilized differential-display
31 TLR4 signaling developed overwhelming, fatal rickettsial infections when given an inoculum that was n
32                      Host cells responded to rickettsial infection with increased secretion of proinf

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