Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
Single-cell RNA profiling suggests goflikicept-mediated immune modulation in idiopathic recurrent pericarditis.
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Golovkin A, Markelova E, Ignatieva E V, Kalinina O, Ivanova O A, Antonets D, Medvedeva Y, Minin A, Shtokalo D, Ramensky V, Kudryavtsev I, Moiseeva O, Myachikova V, Vyatkin Y, Lavrovsky Y, Samsonov M, Maslyanskiy A, Kostareva A, Shlyakhto E
Аннотация
OBJECTIVE: Idiopathic recurrent pericarditis (IRP) is a rare autoinflammatory disorder characterized by NLRP3 inflammasome overactivation, resulting in excessive IL-1β and IL-1α production. Although IL-1 blockade shows promise as a therapeutic strategy, the underlying molecular mechanisms remain incompletely understood. We investigated the effect of goflikicept, a novel heterodimeric fusion protein that inhibits both IL-1β and IL-1α, on peripheral blood mononuclear cell (PBMC) transcriptomes from patients with IRP.
METHODS: Single‑cell RNA sequencing was performed on PBMCs from patients with IRP before and during goflikicept treatment. Treatment‑related transcriptomic signatures were analyzed across innate and adaptive immune cell subsets.
RESULTS: Goflikicept induced temporal transcriptional reprogramming, with a particularly pronounced downregulation of IL-1-related inflammatory pathways in classical monocytes by day 35 of treatment. Furthermore, goflikicept was associated with coordinated transcriptional changes in adaptive immune compartments, including naïve B cells, circulating plasma cell precursors, and unconventional T cell subsets (γδ T and MAIT cells).
CONCLUSIONS: Goflikicept effectively normalized dysregulated immune responses in IRP, supporting the broader therapeutic potential of IL-1 blockade in NLRP3-mediated inflammatory diseases. This study provides the first single-cell resolution insights into the molecular mechanisms of IL-1 blockade, informing the development of targeted therapies for autoinflammatory conditions.
METHODS: Single‑cell RNA sequencing was performed on PBMCs from patients with IRP before and during goflikicept treatment. Treatment‑related transcriptomic signatures were analyzed across innate and adaptive immune cell subsets.
RESULTS: Goflikicept induced temporal transcriptional reprogramming, with a particularly pronounced downregulation of IL-1-related inflammatory pathways in classical monocytes by day 35 of treatment. Furthermore, goflikicept was associated with coordinated transcriptional changes in adaptive immune compartments, including naïve B cells, circulating plasma cell precursors, and unconventional T cell subsets (γδ T and MAIT cells).
CONCLUSIONS: Goflikicept effectively normalized dysregulated immune responses in IRP, supporting the broader therapeutic potential of IL-1 blockade in NLRP3-mediated inflammatory diseases. This study provides the first single-cell resolution insights into the molecular mechanisms of IL-1 blockade, informing the development of targeted therapies for autoinflammatory conditions.