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Cue Biopharma to Present New In vitro Data for CUE-401 at the 20th World Immune Regulation Meeting (WIRM) 2026
BOSTON, March 09, 2026 (GLOBE NEWSWIRE) -- Cue Biopharma, Inc. (Nasdaq: CUE), a clinical-stage biopharmaceutical company developing a novel class of
About this update from Cue Biopharma, Inc.
[{"type":"text","content":"BOSTON, March 09, 2026 (GLOBE NEWSWIRE) -- Cue Biopharma, Inc. (Nasdaq: CUE), a clinical-stage biopharmaceutical company developing a novel class of therapeutic biologics to selectively engage and modulate disease-specific T cells for the treatment of autoimmune and inflammatory diseases, today announced that it will deliver a poster presentation on the company’s lead asset, CUE-401, at the World Immune Regulation Meeting (WIRM) being held March 11-14, 2026 in Davos, Switzerland. The presentation will include new in vitro data that demonstrate the therapeutic potential of CUE-401 to restore immune balance for the treatment of autoimmune and inflammatory diseases. Poster Presentation Session: P5 – Autoimmunity and Innate ImmunityTitle: CUE-401: A Novel Bifunctional TGF-beta/IL-2 Fusion Protein for the Treatment of Autoimmune and Inflammatory DiseasesPresenter: Natasha M. Girgis, Director, Translational PharmacologyDate and Time: Day 2 – Thursday, March 12, 2026, 8:00 p.m.–11:00 p.m. CET, 3:00 p.m.–6:00 p.m. EDT Natasha M. Girgis, Director, Translational Pharmacology will discuss new in vitro data that support CUE-401’s ability to directly inhibit proinflammatory immune cells via the direct effects of TGF-beta (TGF-β). TGF-β is a potent immunoregulatory cytokine that maintains peripheral tolerance by inhibiting diverse types of inflammatory immune cells and proinflammatory pathways, making it an attractive therapeutic target for treating autoimmune and inflammatory diseases. In addition to expanding Tregs, we show that CUE-401 controlled proinflammatory pathways via direct effects of TGF-β on multiple cell types that contribute to autoimmune disease. In CD4+ T effector memory cells, CUE-401 showed TGF-β-dependent suppression of proinflammatory cytokines, including Th1, Th2, and Th17 responses. In addition, the TGF-β in CUE-401 prevented activated B cells from differentiating into plasma cells and limited antibody production. In natural killer (NK) cells, TGF-β in CUE-401 counterbalanced the activating effects of interleukin-2 (IL-2), preventing proliferation and upregulation of proinflammatory cytokine production. Together, we believe these results demonstrate that CUE-401 has the potential to provide both short-term control of diverse inflammatory processes via TGF-β, while also potentially providing durable long-term benefit thr...