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Publication : Mice lacking α1,3-fucosyltransferase 9 exhibit modulation of in vivo immune responses against pathogens.

First Author  Kashiwazaki H Year  2014
Journal  Pathol Int Volume  64
Issue  5 Pages  199-208
PubMed ID  24888773 Mgi Jnum  J:286453
Mgi Id  MGI:6403671 Doi  10.1111/pin.12159
Citation  Kashiwazaki H, et al. (2014) Mice lacking alpha1,3-fucosyltransferase 9 exhibit modulation of in vivo immune responses against pathogens. Pathol Int 64(5):199-208
abstractText  Carbohydrate structures, including Lewis X (Le(x)), which is not synthesized in mutant mice that lack alpha1,3-fucosyltransferase 9 (Fut9(-/-)), are involved in cell-cell recognition and inflammation. However, immunological alteration in Fut9(-/-) mice has not been studied. Thus, the inflammatory response of Fut9(-/-) mice was examined using the highly neurovirulent mouse hepatitis virus (MHV) JHMV srr7 strain. Pathological study revealed that inflammation induced in the brains of Fut9(-/-) mice after infection was more extensive compared with that of wild-type mice, although viral titers obtained from the brains of mutant mice were lower than those of wild-type mice. Furthermore, the reduction in cell numbers in the spleens of wild-type mice after infection was not observed in the infected Fut9(-/-) mice. Although there were no clear differences in the levels of cytokines examined in the brains between Fut9(-/-) and wild-type mice except for interferon-beta expression, some of those in the spleens, including interferon-gamma, interleukin-6, and monocyte chemoattractant protein 1, showed higher levels in Fut9(-/-) than in wild-type mice. Furthermore, Fut9(-/-) mice were refractory to the in vivo inoculation of endotoxin (LPS) compared with wild-type mice. These results indicate that Le(x) structures are involved in host responses against viral or bacterial challenges.
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