ReviewImmunologic research2022
Semaphorin-3A: a promising therapeutic tool in allergic rhinitis.
Review in Immunologic research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Serum Semaphorin Alterations in Psoriasis: Links to Metabolic Status Rather than Disease Severity.Metabolites · 2026Article
- Semaphorin-3A in autoimmune rheumatic diseases: immunological and pathological aspects.Inflammopharmacology · 2025Review
- Knocking down hypoxia-induced Semaphorin 6B may attenuate the progression of cervical cancer through regulating macrophage M2 polarization.Journal of translational medicine · 2025Article
- Sema3A Affect Osteolytic Bone Metastasis of Non-small Cell Lung Cancer.Recent patents on anti-cancer drug discovery · 2025Article
- Conventional DMARDs therapy decreases disease activity and inflammation in newly diagnosed patients with rheumatoid arthritis by increasing FoxP3, Sema-3A, and Nrp-1 gene expression.Inflammopharmacology · 2024Article
- Semaphorin 3 a restores the ability of type 1 regulatory T cells to suppress food allergy.Immunologic research · 2024Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Semaphorin-3A (Sema-3A), a secreted member of the semaphorin family, is well known for playing regulatory functions at all stages of the immune response. Sema-3A transduces signals by binding to its cognate receptors, namely, class A plexins (Plxns A1 to A4) and neuropilin-1 (Nrp-1). The downstream diverse signaling pathways induced by connecting Sema-3A to its receptors were found to be involved in the pathogenesis of different immunological disorders, ranging from cancer to autoimmunity and allergies. Recent studies have demonstrated that Sema-3A expression is diminished in the murine models and patients with allergic rhinitis (AR; a chronic inflammatory disorder of the nasal mucosa), suggesting the involvement of Sema-3A in AR pathogenesis. Investigations also revealed that treatment of these mice with exogenous Sema-3A protein alleviates the clinical symptom scores of AR, thereby compensating for the reduced expression of Sema-3A in AR. Indeed, Sema-3A treatment could suppress allergic responses in AR via inhibiting Th2/Th17 responses and boosting Th1/Treg responses. Also, Sema-3A could diminish dendritic cell (DC) maturation and T cell proliferation. Since it is implicated in the pathogenesis of AR; thus, Sema-3A turns to be a promising tool of therapy to be studied and utilized in this disease. This review intends to highlight the recent evidence on the role of Sema-3A in AR pathogenesis and summarizes the recent findings regarding the expression status of Sema-3A, as well as its therapeutic potential for treating this disease. HIGHLIGHTS: Sema-3A plays regulatory functions at all stages of the immune response. Sema-3A receptors are the class A plexins (A1-A4) and neuropilin-1 (Nrp-1). Sema-3A expression is reduced in murine models and patients with allergic rhinitis. Connecting Sema-3A to Nrp-1 increases Foxp3 expression in Treg cells. Injecting Sema-3A protein exerts therapeutic effects in mouse models of allergic diseases. Sema-3A shows promise as a therapeutic tool for the treatment of allergic rhinitis.
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