Study Pinpoints GPR25 as Switch for Tissue-Resident Memory T Cell Formation

Overview

• La Jolla Institute for Immunology researchers detail the discovery in Science Immunology, building on earlier transcriptomic clues.
• GPR25 is induced by TGF-β and preserves downstream signaling that drives differentiation of tissue-resident memory T cells.
• Knockout mice lacking GPR25 show fading TGF-β signals and fail to form or maintain these cells in the lung and liver.
• As a cell-surface GPCR, GPR25 is presented as a druggable target to enhance organ-specific immunity in cancer or infection or to dampen harmful activity in autoimmune disease.
• The findings are preclinical and derived from mouse models, so human validation and safety assessments remain ahead.