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Scientific Fields
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Published in Nature communications - 24 Nov 2017

Li Y, Strick-Marchand H, Lim AI, Ren J, Masse-Ranson G, Dan Li , Jouvion G, Rogge L, Lucas S, Bin Li , Di Santo JP

Link to Pubmed [PMID] – 29176694

Nat Commun 2017 11;8(1):1762

While patient selection and clinical management have reduced high-dose IL-2 (HDIL2) immunotherapy toxicities, the immune mechanisms that underlie HDIL2-induced morbidity remain unclear. Here we show that dose-dependent morbidity and mortality of IL-2 immunotherapy can be modeled in human immune system (HIS) mice. Depletion of human T cell subsets during the HDIL2 treatment reduces toxicity, pointing to the central function of T cells. Preferential expansion of effector T cells secondary to defective suppressive capacity of regulatory T (T) cells after HDIL2 therapy further underscores the importance of T in the maintenance of immune tolerance. IL-2 toxicity is induced by selective depletion or inhibition of T after LDIL2 therapy, and is ameliorated in HDIL2-treated HIS mice receiving the PIM-1 kinase inhibitor, Kaempferol. Modeling IL-2 pathophysiology in HIS mice offers a means to understand the functions of effector and regulatory T cells in immune-mediated toxicities associated with cancer immunotherapy.

https://www.ncbi.nlm.nih.gov/pubmed/29176694