ArticleInternational archives of allergy and immunology2020
Novel Toll-Like Receptor 9 Agonist Derived from Cryptococcus neoformans Attenuates Allergic Inflammation Leading to Asthma Onset in Mice.
Article in International archives of allergy and immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed, 4 citations in OpenAlex.
- TLR ligands as immunomodulators: mechanistic insights and therapeutic potential in infectious and inflammatory diseases.Molecular biology reports · 2026Review
- BIOMOLECULAR ACTIVITY OF CRYPTOCOCCUS DURING CRYPTOCOCCOSIS: A REVIEW OF MOLECULAR INTERACTIONS OF CRYPTOCOCCUS WITH HUMAN IMMUNE SYSTEM AND BLOOD-BRAIN-BARRIER.African journal of infectious diseases · 2024Article
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Authors and funding
17 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
introductionThe enhanced type 2 helper (Th2) immune response is responsible for the pathogenesis of allergic asthma. To suppress the enhanced Th2 immune response, activation of the Th1 immune response has been an alternative strategy for anti-asthma therapy. In this context, effective Th1-inducing adjuvants that inhibit the development of allergic asthma but do not flare the side effects of the primary agent are required in clinical treatment and preventive medicine.
objectiveIn this study, we aimed to determine the regulation of the Th2 type immune response in asthma by a novel immunostimulatory oligodeoxynucleotide (ODN) derived from Cryptococcus neoformans, termed ODN112, which contains a cytosine-guanine (CG) sequence but not canonical CpG motifs.
methodsUsing an ovalbumin-induced asthma mouse model, we assessed the effect of ODN112 on prototypical asthma-related features in the lung and on the Th1/Th2 profile in the lymph nodes and lung of mice treated with ODN112 during sensitization. RESULTS AND
conclusionODN112 treatment attenuated asthma features in mice. In the bronchial lymph nodes of the lungs and in the spleen, ODN112 increased interferon-γ production and attenuated Th2 recall responses. In dendritic cells (DCs) after allergen sensitization, ODN112 enhanced cluster of differentiation (CD) 40 and CD80 expression but did not alter CD86 expression. Interleukin-12p40 production from DCs was also increased in a Th2-polarizing condition. Our results suggest that ODN112 is a potential Th1-inducing adjuvant during Th2 cell differentiation in the sensitization phase.
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