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1  cells can adoptively transfer resistance to toxoplasmic encephalitis.
2 ncreased brain cyst burdens and succumbed to toxoplasmic encephalitis.
3 ndii infections that invariably cause lethal toxoplasmic encephalitis.
4  to visualize effector CD8(+) T cells during toxoplasmic encephalitis.
5 parable levels of IFN-gamma but succumbed to toxoplasmic encephalitis 4 to 5 weeks after infection.
6 ific for LDH1 that may be useful in treating toxoplasmic encephalitis and other complications that ar
7 re susceptible to disease, developing severe toxoplasmic encephalitis and succumbing within 30 days.
8  signaling is activated in astrocytes during toxoplasmic encephalitis and that inhibition of astrocyt
9 les from 12 patients with AIDS and confirmed toxoplasmic encephalitis (defined as positive mouse inoc
10  however, these mice eventually succumbed to toxoplasmic encephalitis, despite the presence of large
11                         Resistance to murine toxoplasmic encephalitis has been precisely and definiti
12 astrocytes to limit neuroinflammation during toxoplasmic encephalitis have not yet been identified.
13  clinical utility of PCR in the diagnosis of toxoplasmic encephalitis in a resource-poor setting.
14 Toxoplasma gondii can cause life-threatening toxoplasmic encephalitis in immunocompromised individual
15 n be reactivated to develop life-threatening toxoplasmic encephalitis in immunocompromised patients.
16 or severe congenital birth defects and fatal toxoplasmic encephalitis in immunocompromized people.
17 f studies over 20 years mapped resistance to toxoplasmic encephalitis in mice to major histocompatibi
18  treatment, IFN-gamma(-/-) mice succumbed to toxoplasmic encephalitis (TE) and died, whereas control
19 on with Toxoplasma gondii and development of toxoplasmic encephalitis (TE) during the late stage of i
20 ix antigen 1 (MAG1), for predicting incident toxoplasmic encephalitis (TE) in people living with huma
21                                              Toxoplasmic encephalitis (TE) is a life-threatening dise
22                                              Toxoplasmic encephalitis (TE) is an opportunistic infect
23 utant during late chronic infection and in a toxoplasmic encephalitis (TE) mouse model.
24  interleukin-6 (IL-6) in the pathogenesis of toxoplasmic encephalitis (TE) was examined by using IL-6
25 ncy of HLA-DQ antigens in AIDS patients with toxoplasmic encephalitis (TE) were examined.
26  are genetically resistant to development of toxoplasmic encephalitis (TE) when infected with Toxopla
27 hat cytokines may have in the development of toxoplasmic encephalitis (TE), the levels of gamma inter
28 istance of BALB/c mice to the development of toxoplasmic encephalitis (TE).
29 or role in resistance against development of toxoplasmic encephalitis (TE).
30 B7.2 was up-regulated in brains of mice with toxoplasmic encephalitis (TE).
31  CMV disease, extrapulmonary cryptococcosis, toxoplasmic encephalitis, tuberculosis, chronic herpes s
32 ion in the immunocompromised leads to lethal Toxoplasmic encephalitis while in the immunocompetent, t
33             c-Rel(-/-) mice developed severe toxoplasmic encephalitis with increased numbers of paras