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NFIL3-deficient mice develop microbiota-dependent, IL-12/23-driven spontaneous colitis.

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NFIL3 deficiency causes spontaneous colitis in mice, independent of IL-10. This immune dysregulation involves microbiota and IL-12p40, highlighting NFIL3

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Area of Science:

  • Immunology
  • Gastroenterology
  • Molecular Biology

Background:

  • NFIL3 is a transcription factor regulating immune functions, notably repressing IL-12p40 in myeloid cells.
  • NFIL3 is implicated as a susceptibility gene in human inflammatory bowel diseases (IBD).

Purpose of the Study:

  • To investigate the role of NFIL3 in the development of colitis.
  • To elucidate the mechanisms underlying NFIL3-mediated regulation of mucosal homeostasis.

Main Methods:

  • Generation and analysis of Nfil3(-/-) mice, Nfil3/Il10 double-knockout mice, and Nfil3/Rag1 double-knockout mice.
  • Adoptive transfer experiments using CD4(+) T cells.
  • Analysis of Nfil3/Il12b double-deficient mice and germ-free Nfil3(-/-) mice.

Main Results:

  • Nfil3(-/-) mice spontaneously develop colitis, which is microbiota-dependent and IL-10-independent.
  • Lymphocytes are required for colitis development, but innate immune cell defects in Nfil3(-/-) mice contribute significantly.
  • Dysregulation of IL-12b (interleukin-12b) is a central pathogenic event in NFIL3-deficient colitis.

Conclusions:

  • NFIL3 is a critical, microbiota-dependent regulator of mucosal homeostasis.
  • NFIL3 acts independently of IL-10 to control IL-12p40 expression, thereby preventing colitis.
  • Targeting NFIL3 or IL-12b pathways may offer therapeutic strategies for inflammatory bowel diseases.