國家衛生研究院 NHRI:Item 3990099045/8297
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    題名: Inability to resolve specific infection generates innate immunodeficiency syndrome in Xiap-/- mice
    作者: Hsieh, WC;Chuang, YT;Chiang, IH;Hsu, SC;Miaw, SC;Lai, MZ
    貢獻者: Division of Vaccine Research and Development
    摘要: Emerging evidence indicates that innate immunodeficiency syndromes are linked to mutations in innate receptors and to specific infections. X-linked lymphoproliferative syndrome type-2 (XLP-2) is associated with deficiency in X-linked inhibitor of apoptosis protein (XIAP), with poorly understood molecular mechanisms. Here we showed that XIAP-deficiency selectively impaired BCL10-mediated innate responses to dectin-1 ligands, but did not affect responses to various Toll-like receptor (TLR) agonists. Consequently, Xiap-/- mice became highly vulnerable upon Candida albicans infection. The compromised early innate responses led to persistent presence of C. albicans and inflammatory cytokines in Xiap-/- mice. Furthermore, priming of Xiap-/- mice with dectin-1 ligand curdlan alone resulted in XLP-2-like syndromes. Restoration of dectin-1-induced Rac1 activation and phagocytosis by resolvin D1, but not up-regulation of NF-kappaB, rescued Xiap-/- mice from C. albicans lethal infection. Therefore, development of XLP-2 in XIAP-deficient patients could be partly due to sustained inflammation as a consequence of defective BCL10-dependent innate immunity toward specific pathogens. Importantly, our results suggest the potential therapeutic value of resolvin D1 in the treatment of XLP-2 and innate immunodeficiency syndromes.
    日期: 2014-10
    關聯: Blood. 2014 Oct;124(18):2847-2857.
    Link to: http://dx.doi.org/10.1182/blood-2014-03-564609
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0006-4971&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000347458500017
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84908599594
    顯示於類別:[許素菁] 期刊論文

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