Phosphorylation of intracellular signaling molecules in peripheral blood cells from psoriasis patients on originator or biosimilar infliximab

Abstract

Background

Psoriasis vulgaris is a chronic, inflammatory skin disease characterized by a dysregulated immune response and it is associated with substantial systemic comorbidities. Biological drugs like tumor necrosis factor (TNF) inhibitors can ameliorate the disease but are expensive. Biosimilar drugs have the same amino acid sequence as the originator, but differences in manufacturing can affect biological activity, efficacy and tolerability.

Objectives

We aimed to explore potential differences in intracellular phosphorylation of signaling molecules in peripheral blood cells from TNF inhibitor infliximab treated psoriasis patients compared to healthy controls, and to investigate if the phosphorylation pattern was influenced by switching from originator infliximab to biosimilar CT-P13.

Methods

By flow cytometry, we measured phosphorylation of NF-κB, ERK1/2, p38 MAPK and STAT3 before and after TNF stimulation in monocytes and T, B, natural killer and CD3⁺CD56⁺ cells from 25 psoriasis patients treated with infliximab and 19 healthy controls.

Results

At inclusion, phosphorylation levels of peripheral blood mononuclear cells were increased in psoriasis patients compared to healthy controls, even though clinical remission had already been achieved. Phosphorylation levels declined in both patients on originator and biosimilar infliximab during continued treatment. No significant differences were detected between the two medications after 12 months.

Conclusions

Psoriasis patients on infliximab have higher activation levels of PBMC than healthy controls, possibly reflecting systemic inflammation. Switching from originator infliximab to biosimilar CT-P13 did not affect phosphorylation levels or clinical parameters, suggesting that CT-P13 is a non-inferior treatment alternative to originator infliximab.

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