Genetic or therapeutic disruption of the Reelin/Apoer2 signaling pathway improves inflammatory arthritis outcomes

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial inflammation, pannus formation, and progressive joint destruction. The inflammatory milieu in RA drives endothelial cell activation and upregulation of adhesion molecules, thus facilitating leukocyte infiltration into the synovium. Reelin, a circulating glycoprotein previously implicated in endothelial activation and leukocyte recruitment in diseases such as atherosclerosis and multiple sclerosis, has emerged as a potential upstream regulator of these processes. However, its role in RA pathogenesis remains poorly understood. Here, we demonstrate that Reelin levels are markedly elevated in the plasma of both RA patients and mouse models of arthritis, with higher concentrations correlating with greater disease severity. Genetic deletion of the Reelin receptor Apoer2 conferred significant protection against serum transfer arthritis (STA), underscoring the relevance of this pathway in disease progression. Furthermore, therapeutic inhibition of Reelin using the CR-50 antibody yielded robust anti-inflammatory effects in multiple preclinical arthritis models, including STA, K/BxN, and collagen-induced arthritis. Notably, CR-50 treatment not only reduced leukocyte infiltration and synovial inflammation but also mitigated pannus formation. Importantly, these benefits were achieved without the gastrointestinal side effects commonly associated with nonsteroidal anti-inflammatory drugs like diclofenac. Our findings position Reelin as a proinflammatory endothelial biomarker and therapeutic target in RA. By modulating endothelial activation and leukocyte recruitment, anti-Reelin strategies offer an alternative approach to attenuate synovial inflammation and joint damage. These results provide a compelling rationale for further exploration of Reelin-targeted therapies as alternatives to conventional immunosuppressive treatments in RA and other chronic inflammatory diseases.

Authors

Institutions

Publication Details

Journal
Proceedings of the National Academy of Sciences
Published
2025-03-12
DOI
https://doi.org/10.1073/pnas.2418642122
Citations
3
Primary Topic
Cytokine Signaling Pathways and Interactions
Type
article
Field-Weighted Citation Impact
3.14

Funders

Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

Genetic or therapeutic disruption of the Reelin/Apoer2 signaling pathway improves inflammatory arthritis outcomes

Laurent Calvier, David R. Karp, Joachim Herz, Sharon Wu et al.
3 citations
Proceedings of the National Academy of Sciences
Cytokine Signaling Pathways and Interactions
3.14
article

Genetic or therapeutic disruption of the Reelin/Apoer2 signaling pathway improves inflammatory arthritis outcomes

Laurent Calvier, David R. Karp, Joachim Herz, Sharon Wu, Catherine R. Wasser, E. Blair Solow, Bret M. Evers, Maria Z. Kounnas
article en
3 citations

Abstract

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial inflammation, pannus formation, and progressive joint destruction. The inflammatory milieu in RA drives endothelial cell activation and upregulation of adhesion molecules, thus facilitating leukocyte infiltration into the synovium. Reelin, a circulating glycoprotein previously implicated in endothelial activation and leukocyte recruitment in diseases such as atherosclerosis and multiple sclerosis, has emerged as a potential upstream regulator of these processes. However, its role in RA pathogenesis remains poorly understood. Here, we demonstrate that Reelin levels are markedly elevated in the plasma of both RA patients and mouse models of arthritis, with higher concentrations correlating with greater disease severity. Genetic deletion of the Reelin receptor Apoer2 conferred significant protection against serum transfer arthritis (STA), underscoring the relevance of this pathway in disease progression. Furthermore, therapeutic inhibition of Reelin using the CR-50 antibody yielded robust anti-inflammatory effects in multiple preclinical arthritis models, including STA, K/BxN, and collagen-induced arthritis. Notably, CR-50 treatment not only reduced leukocyte infiltration and synovial inflammation but also mitigated pannus formation. Importantly, these benefits were achieved without the gastrointestinal side effects commonly associated with nonsteroidal anti-inflammatory drugs like diclofenac. Our findings position Reelin as a proinflammatory endothelial biomarker and therapeutic target in RA. By modulating endothelial activation and leukocyte recruitment, anti-Reelin strategies offer an alternative approach to attenuate synovial inflammation and joint damage. These results provide a compelling rationale for further exploration of Reelin-targeted therapies as alternatives to conventional immunosuppressive treatments in RA and other chronic inflammatory diseases.

Proceedings of the National Academy of SciencesVol. 122(11)
Rodin Therapeutics (United States) (US), Southwestern Medical Center (US), The University of Texas Southwestern Medical Center (US)
Alzheimer's Association, BrightFocus Foundation, Small Business Innovation Research, Robert J. Kleberg, Jr. and Helen C. Kleberg Foundation, Deutsche Forschungsgemeinschaft, National Institutes of Health, National Institute on Aging, National Heart, Lung, and Blood Institute, National Institute of Arthritis and Musculoskeletal and Skin Diseases
Good health and well-being
Openalex Percentile: Top 9%
Cytokine Signaling Pathways and Interactions
3.14
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.