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1  new insights into the roles of CDPKs during Toxoplasma gondii infection.
2 responses using a mouse model for persistent Toxoplasma gondii infection.
3 immunity exacerbates ileitis induced by oral Toxoplasma gondii infection.
4 osis Study (NCCCTS) have a high incidence of Toxoplasma gondii infection.
5 August 2010 for serologic evidence of recent Toxoplasma gondii infection.
6 3, TLR7, and TLR9, are highly susceptible to Toxoplasma gondii infection.
7 as in response to Listeria monocytogenes and Toxoplasma gondii infection.
8 xpression by CNS-infiltrating T cells during Toxoplasma gondii infection.
9 s important for long-term protection against Toxoplasma gondii infection.
10 otoxin shock, and enhanced susceptibility to Toxoplasma gondii infection.
11 e course of the Th1 inflammatory response to Toxoplasma gondii infection.
12 t mediator for the immune response following Toxoplasma gondii infection.
13 und useful for very early diagnosis of acute Toxoplasma gondii infection.
14 n-15 (IL-15) in resistance to and memory for Toxoplasma gondii infection.
15 that IGTP is critical for host resistance to Toxoplasma gondii infection.
16 are tissue cysts in the eye after 4 weeks of Toxoplasma gondii infection.
17 TL) are part of the human immune response to Toxoplasma gondii infection.
18 f granulocyte responses and pathology during Toxoplasma gondii infection.
19 ion has been reported in mice susceptible to Toxoplasma gondii infection.
20 ne C57BL/6 mice are susceptible to secondary Toxoplasma gondii infection.
21 tions and immune regulation of GDF-15 during Toxoplasma gondii infection.
22 ed immunity, both in vitro and in vivo, upon Toxoplasma gondii infection.
23 on with Dirofilaria repens, Toxocara sp. and Toxoplasma gondii infection.
24 sistance to acute Listeria monocytogenes and Toxoplasma gondii infections.
25                                 Treatment of Toxoplasma gondii infection acquired during pregnancy di
26 re we show that GCs are induced during acute Toxoplasma gondii infection and directly control the T c
27 een dedicated to the laboratory diagnosis of Toxoplasma gondii infection and toxoplasmosis.
28  are known mediators of immune resistance to Toxoplasma gondii infection, but whether B cells also pl
29                                              Toxoplasma gondii infections can cause serious complicat
30 hough important for protection against acute Toxoplasma gondii infection, can cause gut pathology, wh
31                                              Toxoplasma gondii infection causes substantial morbidity
32                            Here, we describe Toxoplasma gondii infection converts NK cells into ILC1-
33 ened mortality after T. cruzi, L. major, and Toxoplasma gondii infection, despite an appropriate IFN-
34 normalities in infants vertically exposed to Toxoplasma gondii infection during an outbreak in Santa
35 et cells, are generated during the course of Toxoplasma gondii infection even in mice lacking the L(d
36                                              Toxoplasma gondii infection has been described previousl
37                                       During Toxoplasma gondii infection, host immunity is mediated b
38 gate the role of interleukin-5 (IL-5) during Toxoplasma gondii infection, IL-5 knockout (KO) mice and
39 sing the BALB/c strain of mice, we show that Toxoplasma gondii infection in a host infected with Heli
40 med to determine whether resistance to acute Toxoplasma gondii infection in mice depends on a mechani
41                                              Toxoplasma gondii infection in mice provides an excellen
42  Tfh-like cells were rapidly generated after Toxoplasma gondii infection in mice, but T-bet constrain
43 ediators of protective host immunity against Toxoplasma gondii infection in mice.
44                                The course of Toxoplasma gondii infection in rats closely resembles th
45 ts use in humans and a good efficacy against Toxoplasma gondii infection in vitro and in mouse models
46 se outcomes associated with the treatment of Toxoplasma gondii infections in patients with various he
47                                      Chronic Toxoplasma gondii infection induces brain-resident CD8+
48                   We show in this study that Toxoplasma gondii infection induces rapid activation of
49                                              Toxoplasma gondii infection is an asymptomatic disease,
50 n, although their role in protection against Toxoplasma gondii infection is not thoroughly understood
51                                 Intrinsic to Toxoplasma gondii infection is the parasite-induced modu
52                         An early hallmark of Toxoplasma gondii infection is the rapid control of the
53 er they develop these characteristics during Toxoplasma gondii infection is unknown.
54                                              Toxoplasma gondii infection is usually benign in Europe
55           The most common method to diagnose Toxoplasma gondii infections is the serological determin
56                        Interestingly, during Toxoplasma gondii infection, KLRG1 is up-regulated on CD
57                                              Toxoplasma gondii infection, like malaria, is sensitive
58 e CD8 T-cell response, these mice succumb to Toxoplasma gondii infection more readily than wild-type
59                                              Toxoplasma gondii infection occurs through the oral rout
60                                              Toxoplasma gondii infection of Alzheimer's disease model
61 eviously showed that IL-1beta release during Toxoplasma gondii infection of primary human monocytes r
62 tion (HMA) is a well-known phenomenon during Toxoplasma gondii infection of the host cell.
63 the epigenomic and transcriptomic effects of Toxoplasma gondii infection on human host cells and demo
64  in NK cells both in vitro and in a model of Toxoplasma gondii infection revealed de novo chromatin a
65 of processes related to the establishment of Toxoplasma gondii infection, such as the formation of th
66 ically highly susceptible to chronic type II Toxoplasma gondii infections that invariably cause letha
67                                       During Toxoplasma gondii infection, the virulence protein TgIST
68                     Thus, we used a model of Toxoplasma gondii infection to investigate whether CD154
69  test this hypothesis in vivo, the course of Toxoplasma gondii infection was assessed in nitric oxide
70 ate immune responses and resistance to acute Toxoplasma gondii infection was assessed in T. gondii-ex
71                    A murine model of peroral Toxoplasma gondii infection was used to determine the co
72 rns of hydrocephalus secondary to congenital Toxoplasma gondii infection were identified and characte
73 LR11, a major TLR involved in recognition of Toxoplasma gondii, infection with this protozoan parasit