{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Abhiraman GC"],"funding":["Howard Hughes Medical Institute","NIAID NIH HHS","Arc Institute Fellowship, Yosemite Innovation Fund","Foundation for the National Institutes of Health","Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.)","Hertz Foundation","NIAMS NIH HHS"],"pagination":["2432"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11897282"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["16(1)"],"pubmed_abstract":["Cytokines are signaling molecules that coordinate complex immune processes and are frequently dysregulated in disease. While cytokine blockade has become a common therapeutic modality, cytokine agonism has had limited utility due to the widespread expression of cytokine receptors with pleiotropic effects. To overcome this limitation, we devise an approach to engineer molecular switches, termed cytokine adaptors, that transform one cytokine signal into an alternative signal with a different functional output. Endogenous cytokines act to nucleate the adaptors, converting the cytokine-adaptor complex into a surrogate agonist for a different cytokine pathway. In this way, cytokine adaptors, which have no intrinsic agonist activity, can function as conditional, context-dependent agonists. We de"],"journal":["Nature communications"],"pubmed_title":["Redirecting immune signaling with cytokine adaptors."],"pmcid":["PMC11897282"],"funding_grant_id":["DP2 AI177915","T32-GM007365","T32 AI007290","T32 AR050942"],"pubmed_authors":["Hsu C","Householder KD","Garcia KC","Glassman CR","Saxton RA","Abhiraman GC","Su L","Wilson SC","Rodriguez GE","Breuer CB","Yen M","Reticker-Flynn NE","Pillarisetty VG"],"additional_accession":[]},"is_claimable":false,"name":"Redirecting immune signaling with cytokine adaptors.","description":"Cytokines are signaling molecules that coordinate complex immune processes and are frequently dysregulated in disease. While cytokine blockade has become a common therapeutic modality, cytokine agonism has had limited utility due to the widespread expression of cytokine receptors with pleiotropic effects. To overcome this limitation, we devise an approach to engineer molecular switches, termed cytokine adaptors, that transform one cytokine signal into an alternative signal with a different functional output. Endogenous cytokines act to nucleate the adaptors, converting the cytokine-adaptor complex into a surrogate agonist for a different cytokine pathway. In this way, cytokine adaptors, which have no intrinsic agonist activity, can function as conditional, context-dependent agonists. We de","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Mar","modification":"2026-06-02T20:51:57.157Z","creation":"2025-04-03T23:57:12.99Z"},"accession":"S-EPMC11897282","cross_references":{"pubmed":["40069219"],"doi":["10.1038/s41467-025-57681-1"]}}