The group investigates cellular and molecular mechanisms of immune dysregulation in inflammatory and autoimmune diseases and inborn errors of immunity. We combine patient-derived material with advanced immunophenotyping, functional assays and experimental models to identify biomarkers of disease activity and potential therapeutic targets.

Group description

The Siedlar Group conducts clinical and translational immunology research focused on the mechanisms of chronic and systemic inflammation and impaired immune-cell function. Particular emphasis is placed on monocytes and macrophages, platelets, lymphocytes and cytokine networks involved in the initiation, maintenance and resolution of inflammatory responses.

A major research area is spondyloarthritis, including axial spondyloarthritis. The group investigates functional immune-cell subsets, the IL-17A–DKK1–VEGF axis and their links to inflammation, angiogenesis and pathological bone remodelling. Patient-derived samples are integrated with in vitro studies and experimental disease models, enabling clinical observations to be connected with molecular mechanisms.

Another important area is the immunology of inborn errors of immunity, with a particular focus on primary humoral immunodeficiencies. The group studies disease mechanisms, diagnostic parameters, treatment responses and long-term consequences of immune dysregulation. This programme is complemented by research on paediatric inflammatory syndromes, including MIS-C, with analyses of cytokine landscapes and therapy-induced changes in immune-cell phenotype and function.

The overarching goal is to define mechanisms that drive pathological inflammation and translate these findings into improved patient stratification, more precise monitoring of disease activity and the identification of new therapeutic targets. The group works closely with clinicians, molecular biologists and teams specialising in multidimensional data analysis.

Main research areas

• Immunopathogenesis of spondyloarthritis and the relationship between inflammation and bone remodelling.
• Heterogeneity and function of monocytes and macrophages in chronic inflammatory diseases.
• The role of platelets, DKK1, VEGF and related mediators in inflammation, angiogenesis and osteogenesis.
• Cytokine and cellular signatures in systemic inflammatory syndromes, including MIS-C.
• Primary humoral immunodeficiencies and other inborn errors of immunity: diagnosis, mechanisms and treatment.
• Development and validation of functional immunological assays and biomarkers of treatment response.

Methods and models

• multiparameter flow cytometry and immune profiling of blood and tissue samples;
• functional assays of monocytes, macrophages, lymphocytes and platelets;
• cytokine, chemokine and regulatory-protein measurements;
• gene-expression analysis, transcriptomic profiling and multidimensional data integration;
• cell culture, differentiation models and pro-inflammatory stimulation assays;
• experimental models of inflammatory disease and bone remodelling;
• clinical-data analysis and discovery of translational biomarkers.

Projects and grants

NCN OPUS 23 – Unexplored role of blood platelet-derived Dickkopf-related protein 1 (DKK1) in the pathomechanism of axial spondyloarthropathy (axSpA).

NCN OPUS 5 – Investigation of the activity of peripheral blood mononuclear cell subpopulations in patients with axial and peripheral spondyloarthritis — pathogenetic implications.

POLNOR-RHEUMA 0026/2019-00 – Personalized medicine in rheumatoid arthritis and spondyloarthritis — integrating clinical and experimental models

Selected publications

2026. Therapy-induced modulation of cellular response in Multisystem Inflammatory Syndrome in Children (MIS-C) — insights into selected immune cells’ markers expression. Scientific Reports. 16(1):21158.  PMID 42103789  DOI 10.1038/s41598-026-47626-z

2026. Neutrophil extracellular traps formation driven by novel ELANE mutations in cyclic neutropenia patients. Genes & Immunity. Opublikowano online 23 czerwca 2026 r. PMID 42337056. DOI 10.1038/s41435-026-00403-4.

2026. Therapy-induced modulation of cellular response in Multisystem Inflammatory Syndrome in Children (MIS-C) – insights into selected immune cells’ markers expression. Scientific Reports. 16(1):21158. PMID 42103789. PMCID PMC13342344. DOI 10.1038/s41598-026-47626-z.

2025. Monoclonal Antibodies Against Vascular Endothelial Growth Factor A (VEGF-A) Reduce Synovitis, Bone Damage, and Osteogenesis in an SKG Mouse Model of Spondyloarthritis. Journal of Immunology Research. 2025:8870895. PMID 40487799. DOI 10.1155/jimr/8870895.

2024. Clinical and experimental treatment of primary humoral immunodeficiencies. Clinical & Experimental Immunology. 216(2):120–131.  PMID 38306460  DOI 10.1093/cei/uxae008

2024. NK-cell receptor modulation in viral infections. Clinical & Experimental Immunology. 217(2):151–158.  PMID 38767592  DOI 10.1093/cei/uxae045

2024. Gene Signature of Regulatory T Cells Isolated from Children with Selective IgA Deficiency and Common Variable Immunodeficiency. Cells. 13(5):417.  PMID 38474381  DOI 10.3390/cells13050417

2024. Cytokine landscape in hospitalized children with multisystem inflammatory syndrome. Scientific Reports. 14:22803.  DOI 10.1038/s41598-024-73956-x

2023. Monocyte subpopulations display disease-specific miRNA signatures depending on the subform of Spondyloarthropathy. Frontiers in Immunology. 14:1124894.  PMID 37138886  DOI 10.3389/fimmu.2023.1124894

2023. Transcriptome profiling of regulatory T cells from children with transient hypogammaglobulinemia of infancy. Clinical & Experimental Immunology. 214(3):275–288.  PMID 37936298  DOI 10.1093/cei/uxad116

2022. Novel IL2RG Gene Mutation in One of Dizygotic Twins Causing Profound Changes of Receptor Structure. Frontiers in Pediatrics. 10:.  PMID 35498802  DOI 10.3389/fped.2022.837388

2021. Role of HMOX1 Promoter Genetic Variants in Chemoresistance and Chemotherapy-Induced Neutropenia in Children with Acute Lymphoblastic Leukemia. International Journal of Molecular Sciences. 22(3):988.  PMID 33498175  DOI 10.3390/ijms22030988

2021. Can we define CD3+CD56+ cells as NKT cells with impunity? Clinical Immunology. 226:108708.  PMID 33662591  DOI 10.1016/j.clim.2021.108708

2021. miRNA Regulation of NK Cells Antiviral Response in Children With Severe and/or Recurrent Herpes Simplex Virus Infections. Frontiers in Immunology. 11:589866.  PMID 33679688  DOI 10.3389/fimmu.2020.589866

2021. Selective downregulation of natural killer activating receptors on NK cells and upregulation of PD-1 expression on T cells in children with severe and/or recurrent Herpes simplex virus infections. Immunobiology. 226(3):152097.  PMID 34015527  DOI 10.1016/j.imbio.2021.152097

2021. Expression of VEGFA-mRNA in classical and MSX2-mRNA in non-classical monocytes in patients with spondyloarthritis is associated with peripheral arthritis. Scientific Reports. 11:9693.  PMID 33958655  DOI 10.1038/s41598-021-89037-2

2021. Down-Regulation of Dkk-1 in Platelets of Patients With Axial Spondyloarthritis. Arthritis & Rheumatology. 73(10):1831–1834.  DOI 10.1002/art.41739

2019. The role of CD44H molecule in the interactions between human monocytes and pancreatic adenocarcinoma-derived microvesicles. Folia Histochemica et Cytobiologica. 57(1):28–34.  PMID 30957871  DOI 10.5603/FHC.a2019.0005

2018. Neurodegenerative changes detected by neuroimaging in a patient with contiguous X-chromosome deletion syndrome encompassing BTK and TIMM8A genes. Central-European Journal of Immunology. 43: [dane strony w rekordzie wydawcy].  DOI 10.5114/ceji.2018.77383

2017. Hyaluronan carried by tumor-derived microvesicles induces IL-10 production in classical (CD14++CD16−) monocytes. Immunobiology. 222(1):1–10.  PMID 26210045  DOI 10.1016/j.imbio.2015.06.019

2017. Comparison of 6B11 monoclonal antibody and α-GalCer-loaded CD1d dextramers for detection of invariant NKT cells. Journal of Immunological Methods. 446:1–6.  PMID 28365328  DOI 10.1016/j.jim.2017.03.016

2017. Alterations of TRIM21-mRNA expression during monocyte maturation. Immunobiology. 222(3):494–498.  PMID 27773663  DOI 10.1016/j.imbio.2016.10.016