ArticleThe Journal of allergy and clinical immunology2013
Clara cell 10-kDa protein inhibits T(H)17 responses through modulating dendritic cells in the setting of allergic rhinitis.
Article in The Journal of allergy and clinical immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 42 citations in OpenAlex.
- Article
- Unraveling the Causal Linkages ofBioMed research international · 2026Article
- Review
- SCGB1A1 as a Key Regulator of Splenic Immune Dysfunction in COPD: Insights From a Murine Model.International journal of chronic obstructive pulmonary disease · 2025Article
- SCGB1A1 as a novel biomarker and promising therapeutic target for the management of HNSCC.Oncology letters · 2024Article
- The multiple facets of the club cell in the pulmonary epithelium.Histology and histopathology · 2024Review
- Clara cell 10 (CC10) protein attenuates allergic airway inflammation by modulating lung dendritic cell functions.Cellular and molecular life sciences : CMLS · 2024Article
- Sex differences in vanadium inhalation effects in non-ciliated bronchiolar cells.Histology and histopathology · 2023Article
- Club Cell Secretory Protein in Lung Disease: Emerging Concepts and Potential Therapeutics.Annual review of medicine · 2023Review
- Characterization of the Notch pathway in nasal polyps of patients with chronic rhinosinusitis: A pilot study.Physiological reports · 2022Article
- Roles of Clara cell 10-kD protein and type 2 innate lymphoid cells in allergic rhinitis.Cell cycle (Georgetown, Tex.) · 2021Article
- Metal exposure from additive manufacturing and its effect on the nasal lavage fluid proteome - a pilot study.PloS one · 2021Article
- Macrophages Inhibit Ciliary Protein Levels by Secreting BMP-2 Leading to Airway Epithelial Remodeling Under Cigarette Smoke Exposure.Frontiers in molecular biosciences · 2021Article
- The role of the non-ciliated bronchiolar cell in tolerance to inhaled vanadium of the bronchiolar epithelium.Histology and histopathology · 2020Article
- Regulatory B cells require antigen recognition for effective allograft tolerance induction.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2020Article
- Expression of Clara cell 10-kDa protein and trefoil factor family 1 in patients with chronic rhinosinusitis and nasal polyps.Experimental and therapeutic medicine · 2018Article
- International Consensus Statement on Allergy and Rhinology: Allergic Rhinitis.International forum of allergy & rhinology · 2018Article
- Clara Cell 10 kDa Protein Alleviates Murine Hepatitis Virus Strain 3-Induced Fulminant Hepatitis by Inhibiting Fibrinogen-Like Protein 2 Expression.Frontiers in immunology · 2018Article
- Neutralization of interleukin-17 suppresses allergic rhinitis symptoms by downregulating Th2 and Th17 responses and upregulating the Treg response.Oncotarget · 2017Article
- Club Cell Protein 16 (CC16) Augmentation: A Potential Disease-modifying Approach for Chronic Obstructive Pulmonary Disease (COPD).Expert opinion on therapeutic targets · 2016Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
Abstract
backgroundT(H)17 responses have recently been implicated to play a role in allergic airway diseases, but their local expression in the setting of allergic rhinitis (AR) and their regulation in allergic airway diseases remain unclear.
objectiveWe sought to investigate the regulatory role of Clara cell 10-kDa protein (CC10), an endogenous regulator of airway inflammation, on T(H)17 responses in the setting of AR.
methodsWild-type and homozygous CC10-null mice were used to establish an ovalbumin (OVA)-induced AR model. Human recombinant CC10 was given during sensitization or challenge. T(H)17 responses in human subjects and mice were examined by using flow cytometry, quantitative RT-PCR assay, immunohistochemistry, and ELISA. The direct effect of CC10 on T(H)17 cells and CD11c(+) dendritic cells (DCs) was studied by means of cell culture. Adoptive transfer was used to examine the influence of CC10-conditioned DCs on airway inflammation. The regulatory effect of CC10 on the expression of the CCL20 gene was tested by using the BEAS-2B cell line.
resultsCompared with those of control subjects, T(H)17 responses were enhanced in the nasal mucosa of patients with AR. CC10-null mice with AR showed enhanced T(H)17 responses, and CC10 treatment significantly decreased T(H)17 responses. CC10 had no direct effect on in vitro T(H)17 cell differentiation. CC10 could significantly decrease the expression of OX40 ligand, IL-23, and IL-6 but enhance CD86 and TGF-β expression in DCs. Importantly, CC10 was able to inhibit T(H)17 cell polarization in the presence of OVA-pulsed DCs. CC10 pretreatment inhibited T(H)17 responses elicited by adoptive transfer of OVA-pulsed DCs. Furthermore, CC10 decreased the expression of CCL20 in BEAS-2B cells induced by inflammatory cytokines.
conclusionT(H)17 responses are enhanced in patients with AR, and CC10 inhibits T(H)17 responses through modulation of the function of DCs.
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