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1 3, TLR7, and TLR9, are highly susceptible to Toxoplasma gondii infection.
2 as in response to Listeria monocytogenes and Toxoplasma gondii infection.
3 xpression by CNS-infiltrating T cells during Toxoplasma gondii infection.
4 s important for long-term protection against Toxoplasma gondii infection.
5 otoxin shock, and enhanced susceptibility to Toxoplasma gondii infection.
6 e course of the Th1 inflammatory response to Toxoplasma gondii infection.
7 t mediator for the immune response following Toxoplasma gondii infection.
8 und useful for very early diagnosis of acute Toxoplasma gondii infection.
9 n-15 (IL-15) in resistance to and memory for Toxoplasma gondii infection.
10 that IGTP is critical for host resistance to Toxoplasma gondii infection.
11 are tissue cysts in the eye after 4 weeks of Toxoplasma gondii infection.
12 TL) are part of the human immune response to Toxoplasma gondii infection.
13 new insights into the roles of CDPKs during Toxoplasma gondii infection.
14 responses using a mouse model for persistent Toxoplasma gondii infection.
15 immunity exacerbates ileitis induced by oral Toxoplasma gondii infection.
16 osis Study (NCCCTS) have a high incidence of Toxoplasma gondii infection.
17 August 2010 for serologic evidence of recent Toxoplasma gondii infection.
18 sistance to acute Listeria monocytogenes and Toxoplasma gondii infections.
20 re we show that GCs are induced during acute Toxoplasma gondii infection and directly control the T c
22 are known mediators of immune resistance to Toxoplasma gondii infection, but whether B cells also pl
24 hough important for protection against acute Toxoplasma gondii infection, can cause gut pathology, wh
26 ened mortality after T. cruzi, L. major, and Toxoplasma gondii infection, despite an appropriate IFN-
27 et cells, are generated during the course of Toxoplasma gondii infection even in mice lacking the L(d
30 gate the role of interleukin-5 (IL-5) during Toxoplasma gondii infection, IL-5 knockout (KO) mice and
31 sing the BALB/c strain of mice, we show that Toxoplasma gondii infection in a host infected with Heli
32 med to determine whether resistance to acute Toxoplasma gondii infection in mice depends on a mechani
33 Tfh-like cells were rapidly generated after Toxoplasma gondii infection in mice, but T-bet constrain
37 n, although their role in protection against Toxoplasma gondii infection is not thoroughly understood
42 e CD8 T-cell response, these mice succumb to Toxoplasma gondii infection more readily than wild-type
44 the epigenomic and transcriptomic effects of Toxoplasma gondii infection on human host cells and demo
45 ically highly susceptible to chronic type II Toxoplasma gondii infections that invariably cause letha
47 test this hypothesis in vivo, the course of Toxoplasma gondii infection was assessed in nitric oxide
48 ate immune responses and resistance to acute Toxoplasma gondii infection was assessed in T. gondii-ex
50 rns of hydrocephalus secondary to congenital Toxoplasma gondii infection were identified and characte
51 LR11, a major TLR involved in recognition of Toxoplasma gondii, infection with this protozoan parasit
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