Bohdana Doskaliuk
Bohdana is an Associate Professor at Ivano-Frankivsk National Medical University. Her PhD research focused on pulmonary involvement in systemic sclerosis and its potential correction.
Bohdana actively contributes also as a reviewer and editor. She serves as an Associate Editor for Rheumatology International and is the Editorial Board member for Therapeutic Advances in Musculoskeletal Disease and Rheumatology Advances in Practice. She is also affiliated with the European Academy of Allergy and Clinical Immunology and European Respiratory Society. Bohdana is a Country Liaison Sub-Committee member.
| Oral OP0251 | Friday 13.06.2025 10.30 Basic Abstract Sessions: Cutting the edges – Omics and new targets in SpA and other inflammatory arthritis Author: Giaglis, S (Switzerland) Title: A cutting-edge three-dimensional stromal-immune microenvironment emulates interactions between synovial fibroblasts and macrophages in inflammatory arthropathies  This study presents a novel 3D organoid model replicating the human synovial microenvironment using patient-derived fibroblasts and macrophages. The model mimics inflammation seen in arthritis and reveals key cytokine responses, offering insights into individual disease mechanisms. It holds promise for personalized therapy development and improves upon the predictive limitations of traditional 2D cultures and animal models. |
| Oral OP0253 | Friday 13.06.25 10:50 Basic Abstract Sessions: Cutting the edges – Omics and new targets in SpA and other inflammatory arthritis Author: Costantino, F (France) Title: Common and rare variant contributions to familial aggregation in spondyloarthritis This abstract investigates genetic contributions to familial spondyloarthritis (SpA). While familial cases showed higher polygenic risk scores and HLA-B27 frequency, these differences disappeared when adjusting for HLA-B27. Rare variant analysis found only a nominal association for the PDE4A gene. Findings suggest that familial aggregation of SpA cannot be fully explained by known common or rare variants, implying roles for other genetic or environmental factors. |
| Poster POS0004 |Wednesday 11.06.25 15:48 Basic and Clinical Poster Tours: Can we stop the fibres? Author: Boleto, G (Portugal) Title: Inhibition of Interleukin-2-Inducible T Cell Kinase with Soquelitinib demonstrates efficacy in preventing lung damage in murine models of systemic sclerosis This study evaluated the ITK inhibitor soquelitinib (SQL) in two mouse models of systemic sclerosis (SSc)-associated lung fibrosis. SQL reduced Th2/Th17 cytokine activity, lung inflammation, fibrosis severity, and pulmonary hypertension markers. These effects were supported by decreased expression of GATA3, RORγt, and MMP2. Results highlight SQL’s potential as a targeted immunotherapy for SSc-related interstitial lung disease, supporting its advancement to clinical trials. |
| Poster POS1368 | Saturday 14.06.2025 10:15 Poster View VIII Author:Solé-Marcé, C (Spain) Title: Topical administration of mirna lipoplexes improves skin lesions in MRL/lpr mice with cutaneous lupus erythematosus. This study demonstrates that topical delivery of anti-miR-31 lipoplexes significantly reduces skin lesions in MRL/lpr mice with cutaneous lupus erythematosus (CLE), outperforming corticosteroids. The treatment showed strong skin localization, minimal systemic distribution, and suppressed miR-31 and NF-κB pathway activity. However, effects were temporary and limited to the skin. These results support lipoplex-based miRNA therapy as a promising localized treatment for CLE. |
| Poster POS1425 | Saturday 14.06.2025 10:15 Poster View VIII Author: Simader, E (Austria) Title: Mediators of osteopetrosis in mir-146a deficient mice This study investigates the mechanisms behind age-related high bone mass in miR-146a-deficient mice. Conditional knockouts revealed that the osteopetrotic phenotype is not driven by T cells, but may involve myeloid cells and is partially mediated by IFN-γ. Notably, IRAK1 deletion completely reversed the high bone mass, highlighting IRAK1 as a key player. These findings provide insight into the role of miR-146a and IRAK1 in bone aging and osteoporosis. |