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- W2890154569 abstract "Inflammatory bowel disease (IBD) are heterogenous disorders of the gastrointestinal tract caused by a spectrum of genetic and environmental factors. In mice, overlapping regions of chromosome 3 have been associated with susceptibility to IBD-like pathology, including a locus called Hiccs. However, the specific gene that controls disease susceptibility remains unknown. Here we identify a Hiccs locus gene, Alpk1 (encoding alpha kinase 1), as a potent regulator of intestinal inflammation. In response to infection with the commensal pathobiont Helicobacter hepaticus (Hh), Alpk1-deficient mice display exacerbated interleukin (IL)-12/IL-23 dependent colitis characterized by an enhanced Th1/interferon(IFN)-γ response. Alpk1 controls intestinal immunity via the hematopoietic system and is highly expressed by mononuclear phagocytes. In response to Hh, Alpk1-/- macrophages produce abnormally high amounts of IL-12, but not IL-23. This study demonstrates that Alpk1 promotes intestinal homoeostasis by regulating the balance of type 1/type 17 immunity following microbial challenge." @default.
- W2890154569 created "2018-09-27" @default.
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- W2890154569 date "2018-09-18" @default.
- W2890154569 modified "2023-10-15" @default.
- W2890154569 title "Alpha kinase 1 controls intestinal inflammation by suppressing the IL-12/Th1 axis" @default.
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- W2890154569 doi "https://doi.org/10.1038/s41467-018-06085-5" @default.
- W2890154569 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6143560" @default.
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