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Differential Roles for Interleukin-23 and Interleukin-17 in Intestinal Immunoregulation.

Joseph R Maxwell1, Yu Zhang1, William A Brown1

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Interleukin-23 (IL-23) inhibition reduces colitis by decreasing inflammation and increasing regulatory T cells. However, blocking IL-17A or IL-17RA worsens colitis by weakening the intestinal barrier.

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Area of Science:

  • Immunology
  • Gastroenterology

Background:

  • Interleukin-23 (IL-23) and Interleukin-17 (IL-17) are key cytokines in inflammatory diseases.
  • Targeting IL-23 and IL-17 pathways shows promise for conditions like psoriasis and Crohn's disease.

Purpose of the Study:

  • To investigate the differential roles of IL-23 and IL-17 in a mouse model of colitis.
  • To elucidate the mechanisms behind the opposing effects of IL-23 and IL-17 inhibition in inflammatory bowel disease.

Main Methods:

  • Utilized the multidrug resistance-1a-ablated (Abcb1a(-/-)) mouse model to study colitis.
  • Administered inhibitors targeting IL-23, IL-17A, or IL-17 receptor A (IL-17RA).
  • Assessed colonic inflammation, regulatory T cell (Treg) populations, and intestinal epithelial barrier integrity.

Main Results:

  • IL-23 inhibition attenuated colitis, reducing inflammation and promoting Treg accumulation.
  • Inhibition of IL-17A or IL-17RA exacerbated colitis, leading to a compromised intestinal epithelial barrier.
  • Barrier dysfunction correlated with increased colonic inflammation and mortality in IL-17-inhibited mice.

Conclusions:

  • IL-17A plays a crucial role in maintaining intestinal epithelial barrier function.
  • The dichotomy in response to IL-23 and IL-17 inhibition highlights distinct therapeutic strategies for inflammatory bowel diseases.
  • Findings provide insights into why IL-17A or IL-17RA inhibition can worsen Crohn's disease.