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  • 1
    Online Resource
    Online Resource
    S. Karger AG ; 2011
    In:  Journal of Innate Immunity Vol. 3, No. 3 ( 2011), p. 264-273
    In: Journal of Innate Immunity, S. Karger AG, Vol. 3, No. 3 ( 2011), p. 264-273
    Abstract: Recent progress in understanding the outcomes of pattern-recognition by myeloid dendritic cells (mDC) allows us to delineate the pathways driving natural killer (NK) cell activation. Mouse mDC mature in response to microbial patterns and are converted to an NK cell-activating phenotype. The MyD88 pathway, the Toll/IL-1 receptor homology domain-containing adaptor molecule (TICAM)-1 (TRIF) pathway, and the interferon (IFN)-β promoter stimulator 1 (IPS-1) pathway in mDC participate in driving NK activation, as shown by analyses in knockout mice. Studies using synthetic compounds for Toll-like receptors/RIG-I-like receptors have demonstrated that mDC-NK cell contact induces NK cell activation without the participation of cytokines in mice. In vivo bone marrow transplantation analysis revealed that the IPS-1 pathway in nonmyeloid cells and the TICAM-1 pathway in mDC are crucial for dsRNA-mediated in vivo NK activation. These results infer the presence of cytokine-dependent and cytokine-independent modes of NK activation in conjunction with innate immune activation. Here, we focus on the IFN-inducing pathways and mDC-NK contact-induced NK activation and discuss the reported various NK activation modes.
    Type of Medium: Online Resource
    ISSN: 1662-811X , 1662-8128
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2011
    detail.hit.zdb_id: 2455818-7
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  • 2
    In: International Archives of Allergy and Immunology, S. Karger AG, Vol. 181, No. 9 ( 2020), p. 651-664
    Abstract: 〈 b 〉 〈 i 〉 Introduction: 〈 /i 〉 〈 /b 〉 The 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. 〈 b 〉 〈 i 〉 Objective: 〈 /i 〉 〈 /b 〉 In this study, we aimed to determine the regulation of the Th2 type immune response in asthma by a novel immunostimulatory oligodeoxynucleotide (ODN) derived from 〈 i 〉 Cryptococcus neoformans 〈 /i 〉 , termed ODN112, which contains a cytosine-guanine (CG) sequence but not canonical CpG motifs. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 Using 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. 〈 b 〉 〈 i 〉 Results and Conclusion: 〈 /i 〉 〈 /b 〉 ODN112 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.
    Type of Medium: Online Resource
    ISSN: 1018-2438 , 1423-0097
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2020
    detail.hit.zdb_id: 1482722-0
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