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Alpha kinase 1 controls intestinal inflammation by suppressing the IL-12/Th1 axis
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Journal Article
Alpha kinase 1 controls intestinal inflammation by suppressing the IL-12/Th1 axis
2018
Overview
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.
The
Hiccs
locus has been associated with susceptibility to colitis in mice. Here the authors identify a
Hiccs
locus gene encoding Alpha kinase 1 as a potent regulator of intestinal inflammation via modulation of the IL-12/Th1 axis.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
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/ 96/95
/ Animals
/ Colitis
/ Colon
/ Female
/ Helicobacter hepaticus - immunology
/ Helicobacter Infections - immunology
/ Helicobacter Infections - microbiology
/ Helicobacter Infections - pathology
/ Humanities and Social Sciences
/ Humans
/ Immunity
/ Inflammatory Bowel Diseases - immunology
/ Inflammatory Bowel Diseases - microbiology
/ Inflammatory Bowel Diseases - pathology
/ Loci
/ Male
/ Mice
/ Protein Kinases - immunology
/ Protein Kinases - metabolism
/ Rodents
/ Science
