Leukemia · 2026
Intracellular IL-23R is necessary for mitotic spindle formation and viability in AML.
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Duong Nathan, Khan Dilshad H, Thomas Geethu E, Feng Yue, Hurren Rose, Lee Jong Bok, St-Germain Jonathan, Drimmer Lily, Yan Yongran, Zhang Lan Xin, Fang Karen Kai-Lin, Ling Dakai, Ma Mary L, MacLean Neil, Gronda Marcela, Rondeau Vincent, Brown Brandon D, Matellán Laura, Jones Courtney L, Chang Hong, Arruda Andrea, Xie Stephanie, Pelletier Laurence, Minden Mark D, Zhang Li, Kornblau Steven M, Raught Brian, Jacobs Kevin, Jacobs Max G, Goede Daniel, Spadavecchio Vito, Schimmer Aaron D
Аннотация
Interleukin-23 receptor (IL-23R) is a cell surface cytokine receptor classically expressed on T cells, where it regulates T cell activation. Here, we discovered a novel intracellular localization and function for IL-23R in Acute Myeloid Leukemia (AML). Compared to normal hematopoietic cells, IL-23R was increased in primary AML samples. IL-23R was predominantly localized intracellularly in AML cells. BioID mass spectrometry identified mitotic spindle proteins as top interactors with IL-23R. We confirmed interaction between endogenous IL-23R and the mitotic spindle in AML cells and primary AML samples, and this interaction was mediated by IL-23R's (S/T)x(I/L)P motif. Genetic depletion of IL-23R disrupted mitotic spindle formation and reduced proliferation and stem cell/progenitor function of AML cell lines and primary AML samples. In contrast, depletion of IL-23R spared normal hematopoietic cells and progenitors. Thus, we discovered a novel intracellular function for IL-23R where this receptor regulates mitotic spindle formation and the growth of AML cells.