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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Host resistance against Listeria monocytogenes is reciprocal during the course of infection in alymphoplastic aly mutant mice.

The aly is a unique spontaneous autosomal recessive mutation in mice that causes a systemic defect of lymph nodes and Peyer's patches. We investigated host resistance against Listeria monocytogenes infection in the mutant. The 50% lethal dose of L. monocytogenes in aly/aly mice was 10-fold higher than their heterozygotes, termed aly/+mice, or their wild-type C57BL/6 mice. The bacterial growth in the spleens and livers of aly/aly mice was more efficient early in infection, and their listericidal activity of peritoneal macrophages was higher than those of aly/+mice. In contrast, the complete elimination of bacteria from the spleens and livers of infected mice in the late stage of infection, in which a T-cell-dependent mechanism is required, was delayed in the aly/aly mice. Moreover, an acquired resistance against secondary infection with L. monocytogenes was markedly diminished in the aly/aly mice. The production of endogenous interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha), which are critical in antilisterial resistance, was reduced in the aly/aly mice during the infection. The production of IFN-gamma, and interleukin-4 was also diminished in the spleen cell cultures of aly/aly mice when stimulated with heat-killed L. monocytogenes or the T-cell receptors were directly stimulated with anti-CD3-epsilon monoclonal antibody. These results suggest that acquired immunity against L. monocytogenes infection is attenuated in aly/aly mice, and that the insufficient production of IFN-gamma and TNF-alpha might be involved in the immunodeficiency.[1]

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