microtis media/悪性腫瘍

A comparative study was done using J774A.1 and J774A.1-derived transfected cells (J774A.1 C.1) containing antisense tumor necrosis factor alpha (TNF-alpha) plasmid to determine the role of endogenous TNF-alpha on nitric oxide production as well as on the growth of Mycobacterium microti in interferon

The growth of Mycobacterium microti was inhibited within J774A.1 macrophage cells activated with either interferon-gamma or tumor necrosis factor-alpha. Activation with interferon-gamma or tumor necrosis factor-alpha alone did not stimulate the production of nitrite in J774A.1 cells.

Pathogens and cancer cells employ the programmed cell death-Ligand 1 (PD-L1)/ programmed cell death-1 (PD-1) signaling pathway to inhibit the immune response. Hence, blockade of PD-L1/PD-1 recognition through monoclonal antibodies enhances the immune response. Antibodies that block PD-L1 and PD-1

Sex-based-differences are known to affect susceptibility to protozoan infections, but their effects on parasitemia and clinical symptoms in Babesia infections remain unclear. We examined the sex-based susceptibility of various mouse strains to Babesia microti Munich strain infection. In all strains,

To investigate effects of Babesia infection on drug metabolism, we intraperitoneally inoculated B. microti into ICR mice and measured the expression and activity of hepatic cytochrome P450 (CYP) 3A, a major drug-metabolizing enzyme. Twelve days after infection, CYP3A11 mRNA, CYP3A protein and

Cord factor (trehalose 6-6' dimycolate). COAM (chlorite-oxidized oxyamylose), zymosan, glucan, Salmonella enteritidis 11RX and Listeria monocytogenes were found to protect mice against subsequent infection with Babesia microti, an intra-erythrocytic protozoan parasite. This protection was not

Babesia microti produces a self-limiting infection in mice, and recovered mice are resistant to reinfection. In the present study, the role of T cells in protective immunity against challenge infection was examined. BALB/c mice which recovered from primary infection showed strong protective immunity

In the present study, we examined the contributions of macrophages to the outcome of infection with Babesia microti, the etiological agent of human and rodent babesiosis, in BALB/c mice. Mice were treated with clodronate liposome at different times during the course of B. microti infection in order