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Updated: Feb 28, 2026

Induction and Diverse Assessment Indicators of Experimental Autoimmune Encephalomyelitis
Published on: September 9, 2022
Ingested (oral) anti-IL-12/23 inhibits EAE
1Department of Neurology, Division of MS/Neuroimmunology, Medical College of Wisconsin, 8701 W Watertown Plank Rd, Milwaukee, WI 53226, USA.
Background:
Blocking the activity of IL-12/23 can inhibit autoimmune diseases such as psoriasis.
Objective:
We examined whether an antibody against IL-12/23, ustekinumab (UTZ) (Stelera®), used clinically in psoriasis would have similar anti-inflammatory effects in EAE after oral administration.
Design/Methods:
B6 mice were immunized with MOG peptide 35-55 and gavaged with isotype IgG control or UTZ during ongoing disease. Splenocytes, CD4(+) T cells or macrophages/monocyte lineage cells (CD11b(+)) from control fed or UTZ fed mice were adoptively transferred into active MOG peptide 35-55 immunized recipient mice during ongoing disease. Actively fed and recipient mice were examined for disease inhibition, inflammation, and cytokine responses.
Results:
Ingested (oral) UTZ inhibited ongoing disease and decreased inflammation. Adoptively transferred cells from UTZ fed donors protected against actively induced disease and decreased inflammation. Oral UTZ decreased pro-inflammatory cytokines Th1-like cytokines IL-2, IL-12, IFN-γ, IL-17 (Teff) and TNF-α in UTZ fed mice and increased counter-regulatory cytokines IL-4, IL-10 and IL-13 in recipients of donor cells from UTZ fed mice.
Conclusions:
Ingested (orally administered) UTZ can inhibit disease, CNS inflammation, decrease pro-inflammatory Th1-like and Th17 cytokines and increase Th2-like anti-inflammatory cytokines.

