ArticleFrontiers in immunology2022
Exogenous Semaphorin 3E treatment protects against chlamydial lung infection in mice.
Article in Frontiers in immunology, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Semaphorin 3E regulates the response of regulatory T cells to lipopolysaccharide-induced systemic inflammation.ImmunoHorizons · 2026Article
- Diverse Roles of Semaphorins on T Cell Activation, Differentiation, Migration, and Effector Functions.Cells · 2026Review
- Engineering CCR2/IFN-γ overexpression in enucleated mesenchymal stem cells enhances therapy for rheumatoid arthritis.Communications biology · 2025Article
- Uncovering genomic diversity and signatures of selection in red Angus × Chinese red steppe crossbred cattle population.Scientific reports · 2025Article
- Th17/Treg Imbalance: Implications in Lung Inflammatory Diseases.International journal of molecular sciences · 2023Review
- Semaphorins in immune cell function, inflammatory and infectious diseases.Current research in immunology · 2023Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies reported that semaphorins play a significant role in various settings of the immune response. In particular, Semaphorin 3E (Sema3E), a secreted semaphorin protein, is involved in cell proliferation, migration, inflammatory responses, and host defence against infections. However, the therapeutic function of Sema3E in bacterial infection has not been investigated. Our data showed that exogenous Sema3E treatment protects mice from chlamydial infection with lower bacterial burden, reduced body weight loss, and pathological lung changes. Cytokine analysis in the lung and spleen revealed that Sema3E-Fc treated mice, compared to saline-Fc treated mice, showed enhanced production of IFN-γ and IL-17 but reduced IL-4 and IL-10 production. Cellular analysis showed that Sema3E treatment leads to enhanced Th1/Th17 response but reduced Treg response in lungs following chlamydial infection. Moreover, Sema3E treatment also enhanced the recruitment of pulmonary dendritic cells, which express higher co-stimulatory but lower inhibitory surface molecules. The data demonstrate that Sema3E plays a vital role in protective immunity against chlamydial lung infection, mainly through coordinating functions of T cells and DCs.
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Registered trials
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