Immunoreactivity profile of peripheral blood mononuclear cells from patients with ragweed‐induced allergic rhinitis
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SummaryBackground
Seasonal rhinitis is manifested by a series of nasal symptoms in response to exposure to seasonal allergens including ragweed pollen. Understanding its immunological mechanisms may help to better manage the disease.Objective
We sought to determine comprehensively ragweed‐induced cytokine and chemokine production by peripheral blood mononuclear cells from normal individuals and patients with seasonal rhinitis sensitized to ragweed pollen, and to assess its regulation by exogenous IL‐10.Methods
Cells were cultured in the presence or absence of a purified ragweed pollen extract with or without exogenous IL‐10. Cytokines and chemokines were measured in the supernatant. Gene expression was evaluated using real‐time quantitative reverse transcription PCR.Results
Ragweed stimulation significantly increased the production of the Th2‐associated cytokines IL‐5, IL‐9 and IL‐13, the chemokines CCL17 and CCL22 and the regulatory cytokine IL‐10 in allergic patients, whereas transforming growth factor‐β (TGF‐β) production was increased only in normal individuals. No difference was detected between groups in the production of the Th1 cytokine IFN‐γ or the Th1‐affiliated chemokines CXCL10 and CXCL11. Exogenous IL‐10 significantly suppressed spontaneous and induced production of both Th1‐ and Th2‐associated cytokines and chemokines.Conclusion
Our work demonstrated that locally manifested allergic rhinitis is underlined by a systemic Th2 immune response specific to allergens. The molecular pathogenesis of allergic rhinitis may be linked to a compromised allergen‐specific immune regulation, e.g., reduced spontaneous and allergen‐induced TGF‐β production in patients compared with healthy controls. Our data also show that IL‐10 inhibits both the effector and directional mechanisms of allergen‐specific immune response, further supporting its potential therapeutic benefit in preventing and treating allergic diseases.
