ArticlePathology international2014
Mice lacking α1,3-fucosyltransferase 9 exhibit modulation of in vivo immune responses against pathogens.
Article in Pathology international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- Integrative multi-omics analysis identified FUT9 and MS4A3 as novel immune-phenotype and prognosis biomarkers for colorectal cancer and analyze the role of FUT9 in oncoimmunology.Scientific reports · 2026Article
- Structure, function, and implications of fucosyltransferases in health and disease.Nature communications · 2025Review
- Effect and Mechanism Analysis of PigInternational journal of molecular sciences · 2022Article
- Dynamic Transcriptome Reveals the Mechanism of Liver Injury Caused by DHAV-3 Infection in Pekin Duck.Frontiers in immunology · 2020Article
- Increased Expression of Cell Surface SSEA-1 is Closely Associated with Naïve-Like Conversion from Human Deciduous Teeth Dental Pulp Cells-Derived iPS Cells.International journal of molecular sciences · 2019Article
- IL-10 expression in pyramidal neurons after neuropathogenic coronaviral infection.Neuropathology : official journal of the Japanese Society of Neuropathology · 2017Article
- Formation of fibroblastic reticular network in the brain after infection with neurovirulent murine coronavirus.Neuropathology : official journal of the Japanese Society of Neuropathology · 2016Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Carbohydrate structures, including Lewis X (Le(x)), which is not synthesized in mutant mice that lack α1,3-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-β expression, some of those in the spleens, including interferon-γ, 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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