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. Author manuscript; available in PMC: 2024 Jul 1.
Published in final edited form as: Nat Rev Gastroenterol Hepatol. 2023 Apr 17;20(7):433–446. doi: 10.1038/s41575-023-00768-1

Table 1 |.

Role of IL-23 in mucosal homeostasis and disease

Cell type Pathway and/ or signalling molecules Effect
Innate immune system
Type 3 innate lymphoid cell IL-23R/STAT5 Cell activation
Cytokine production (IL-17A, IL-22)
Antimicrobial effects
Granulocyte IL-23R Cell activation
Pro-inflammatory cytokine production
Natural killer/intraepithelial lymphocytes IL-23R Cytotoxicity
Cell activation
Pro-inflammatory cytokine production
Adaptive immune system
Treg Cells,
Teff cells,
TH17 cells
IL-23R
RORγt (Teff cells)
Suppression of Treg cells
Proliferation and expansion of TH17 cells
Production of IL-6 and TH17 cytokines
Intestinal epithelial cells IL-22 Regenerating gene family proteins Increased barrier function
Antimicrobial effects

Interleukin-23 (IL-23) exerts effects on both innate and adaptive immune cells. In type 3 innate lymphoid cells, granulocytes, intraepithelial lymphocytes and natural killer cells, IL-23 induces cell activation and cytokine production. Additional effects of IL-23 are related to adaptive immune cells, such as regulatory T (Treg) cells, and effector T (Teff) cells, such as T helper 17 (TH17) cells. In this context, IL-23 suppresses Treg cells, whereas it activates TH17 cells. Furthermore, this cytokine regulates barrier function and production of antimicrobial peptides in intestinal epithelial cells. IL-23R, IL-23 receptor; RORγt, retinoid-related orphan receptor-γt; STAT, signal transducer and activator of transcription.