ArticleSkeletal muscle2015
CD49d is a disease progression biomarker and a potential target for immunotherapy in Duchenne muscular dystrophy.
Article in Skeletal muscle, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 29 citations in OpenAlex.
- Trial
- Sustained monocyte activation by persistent challenges with either oxLDL or free cholesterol and underlying mechanisms.ImmunoHorizons · 2026Article
- The Gut Microbiota Involvement in the Panorama of Muscular Dystrophy Pathogenesis.International journal of molecular sciences · 2024Review
- Association between blood eosinophil count and Duchenne muscular dystrophy severity and prognosis: a retrospective cohort study.Italian journal of pediatrics · 2023Article
- Recent Trends in Antisense Therapies for Duchenne Muscular Dystrophy.Pharmaceutics · 2023Review
- T cell biology in neuromuscular disorders: a focus on Duchenne Muscular Dystrophy and Amyotrophic Lateral Sclerosis.Frontiers in immunology · 2023Review
- A Spotlight on T Lymphocytes in Duchenne Muscular Dystrophy-Not Just a Muscle Defect.Biomedicines · 2022Review
- Multi-Modal Single-Cell Sequencing Identifies Cellular Immunophenotypes Associated With Juvenile Dermatomyositis Disease Activity.Frontiers in immunology · 2022Article
- Integrin-directed antibody-based immunotherapy: focus on VLA-4.Immunotherapy advances · 2021Review
- Laminin-111 protein therapy after disease onset slows muscle disease in a mouse model of laminin-α2 related congenital muscular dystrophy.Human molecular genetics · 2020Article
- Crosstalk Between Innate and T Cell Adaptive Immunity With(in) the Muscle.Frontiers in physiology · 2020Review
- Reduction of integrin alpha 4 activity through splice modulating antisense oligonucleotides.Scientific reports · 2019Article
- HGF potentiates extracellular matrix-driven migration of human myoblasts: involvement of matrix metalloproteinases and MAPK/ERK pathway.Skeletal muscle · 2017Article
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Authors and funding
19 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDuchenne muscular dystrophy (DMD) is caused by mutations in the dystrophin gene. The immune inflammatory response also contributes to disease progression in DMD patients. In a previous study, we demonstrated higher levels of circulating CD49dhi and CD49ehi T cells in DMD patients compared to healthy control. DMD patients are clinically heterogeneous and the functional defect cannot be correlated with genotype. Therefore, it is important to be able to define reliable noninvasive biomarkers to better define the disease progression at the beginning of clinical trials.
resultsWe studied 75 DMD patients at different stages of their disease and observed that increased percentages of circulating CD4(+)CD49d(hi) and CD8(+)CD49d(hi) T lymphocytes were correlated with both severity and a more rapid progression of the disease. Moreover, T(+)CD49d(+) cells were also found in muscular inflammatory infiltrates. Functionally, T cells from severely affected patients exhibited higher transendothelial and fibronectin-driven migratory responses and increased adhesion to myotubes, when compared to control individuals. These responses could be blocked with an anti-CD49d monoclonal antibody.
conclusionCD49d can be used as a novel biomarker to stratify DMD patients by predicting disease progression for clinical trials. Moreover, anti-CD49d peptides or antibodies can be used as a therapeutic approach to decrease inflammation-mediated tissue damage in DMD.
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