PhD Scientific Days 2026

Budapest, 16-18 June 2026

Poster Session 2.C - Molecular Medicine

Lymphatic Ablation Drives Severe Autoimmune Arthritis via Immune Complex-Mediated Inflammation

Előadó neve

Kovács-Kemecsei, Éva

Neptune code

CHFPOY

Előadó munkahelye

Department of Physiology, Semmelweis University, Budapest, Hungary

Előadó telefonszáma

06301808944

Előadó e-mail címe

kemecsei.eva@semmelweis.hu

Az előadás címe

Lymphatic Ablation Drives Severe Autoimmune Arthritis via Immune Complex-Mediated Inflammation

Szerző(k) neve és munkahelye

Éva Kovács-Kemecsei1, Gábor Kovács1, Stella Márta Sági1, Kornél Molnár1, Petra Aradi1, Mohsen Pourmohammad1, Dániel Csete1, Attila Mócsai1, Raghu P. Kataru2, Babak J. Mehrara2, Zoltán Jakus1

1: Department of Physiology, Semmelweis University, Budapest, Hungary
2: Department of Surgery, Division of Plastic and Reconstructive Surgery, Memorial Sloan Kettering Cancer Center, New York, NY, USA

Bemutatás módja

Poszter

Szekció

Poster Session 2.C - Molecular Medicine

Language of the presentation

English

Preferred session

Molecular Medicine

Összefoglaló szövege

Introduction: Rheumatoid arthritis is a chronic autoimmune disorder, primarily affecting the small joints. Despite the known connection between the immune and lymphatic systems, the role of lymphatics in autoimmune arthritis remains unclear.
Aims: Our aim was to investigate the mechanisms by which lymphatic vessels influence the effector phase of autoimmune arthritis.
Methods: Diphtheria toxin-mediated ablation of the local lymphatic vasculature was induced in the hindlimbs of a transgenic mouse model, followed by the induction of arthritis via K/BxN serum transfer. Disease progression was monitored by ankle thickness measurement and clinical scoring. Hindlimb samples were processed for histology, and peripheral autoantibody and local immune-complex levels were measured by ELISA. Local immune cell populations were quantified by flow cytometry, and arthritis-associated bone alterations were assessed by micro-CT.
Results: Lymphatic-deficient mice developed arthritis earlier and displayed more severe progression compared with controls. Histological and micro-CT analysis revealed significantly exacerbated bone erosion and structural damage in lymphatic-deficient arthritic mice. Peripheral autoantibody levels showed no significant differences between arthritic groups. In contrast, local immune-complex accumulation was markedly elevated in lymphatic-deficient arthritic mice, accompanied by a substantial increase in neutrophil infiltration.
Conclusion: Our findings indicate that the local lymphatic vasculature plays a critical immunomodulatory role in the effector phase of autoimmune arthritis. Loss of lymphatic vessels exacerbated autoimmune arthritis, possibly driven by impaired clearance. These results suggest that therapeutic strategies aimed at preserving or enhancing lymphatic function may hold promise in the treatment of autoimmune arthritis.
Funding: National Research, Development and Innovation Office (K139165, TKP2021-EGA-29, TKP2021-EGA-24, 2023-1.2.4-TÉT-2023-00053, 2025-1.2.1-HU-RIZONT-2025-00028), the European Union and the Hungarian Government (VEKOP-2.3.2-16-2016-00002, VEKOP-2.3.3-15-2016-00006), Semmelweis University (STIA-MEC22), Predoctoral Research Fund of the Semmelweis University, Z.J. was a recipient of the János Bolyai Research Scholarship of the Hungarian Academy of Sciences (BO/00898/22)

University

Semmelweis University

Other university, not listed above

-

Supervisor

Dr. Zoltán Jakus

Publication of my abstract

I do not give consent to the publication of my abstract on the website of the congress.

phd.section.field

after finishing doctoral studies with absolutorium (PhD)

Kind

Szabad

Status

elfogadva

Accepted presentation method

poszter

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

6128

Start

18:30

End

18:33