Site-specific PEGylation of interleukin-2 enhances immunosuppression via the sustained activation of regulatory T cells

Zhang, B., Sun, J., Wang, Y., Ji, D., Yuan, Y., Li, S., Sun, Y., Hou, Y., Li, P., Zhao, L., Yu, F., Ma, W., Cheng, B., Wu, L., Hu, J., Wang, M., Song, W., Li, X., Li, H., … Zhang, X. (2021). Site-specific PEGylation of interleukin-2 enhances immunosuppression via the sustained activation of regulatory T cells. Nat Biomed Eng, 5, 1288-1305.

Abstract

The preferential activation of regulatory T (T(reg)) cells by interleukin-2 (IL-2), which selectively binds to the trimeric IL-2 receptor (IL-2R) on T(reg) cells, makes this cytokine a promising therapeutic for the treatment of autoimmune diseases. However, IL-2 has a narrow therapeutic window and a short half-life. Here, we show that the pharmacokinetics and half-life of IL-2 can be substantially improved by orthogonally conjugating the cytokine to poly(ethylene glycol) (PEG) moieties via a copper-free click reaction through the incorporation of azide-bearing amino acids at defined sites. Subcutaneous injection of a PEGylated IL-2 that optimally induced sustained T(reg)-cell activation and expansion over a wide range of doses through highly selective binding to trimeric IL-2R led to enhanced therapeutic efficacy in mouse models of lupus, collagen-induced arthritis and graft-versus-host disease without compromising the immune defences of the host against viral infection. Site-specific PEGylation could be used more generally to engineer cytokines with improved therapeutic performance for the treatment of autoimmune diseases.
Last updated on 02/17/2024