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Type I IFN signaling in CD8– DCs impairs Th1-dependent malaria immunity

หน่วยงาน Nanyang Technological University, Singapore

รายละเอียด

ชื่อเรื่อง : Type I IFN signaling in CD8– DCs impairs Th1-dependent malaria immunity
นักวิจัย : Haque, Ashraful , Best, Shannon E. , Montes de Oca, Marcela , James, Kylie R. , Ammerdorffer, Anne , Edwards, Chelsea L. , de Labastida Rivera, Fabian , Amante, Fiona H. , Bunn, Patrick T. , Sheel, Meru , Sebina, Ismail , Koyama, Motoko , Varelias, Antiopi , Hertzog, Paul J. , Kalinke, Ulrich , Gun, Sin Yee , Rénia, Laurent , Ruedl, Christiane , MacDonald, Kelli P.A. , Hill, Geoffrey R. , Engwerda, Christian R.
คำค้น : DRNTU::Science::Medicine
หน่วยงาน : Nanyang Technological University, Singapore
ผู้ร่วมงาน : -
ปีพิมพ์ : 2557
อ้างอิง : Haque, A., Best, S. E., Montes de Oca, M., James, K. R., Ammerdorffer, A., Edwards, C. L., et al. (2014). Type I IFN signaling in CD8– DCs impairs Th1-dependent malaria immunity. Journal of Clinical Investigation, 124(6), 2483-2496. , 0021-9738 , http://hdl.handle.net/10220/20014 , http://dx.doi.org/10.1172/JCI70698
ที่มา : -
ความเชี่ยวชาญ : -
ความสัมพันธ์ : Journal of clinical investigation
ขอบเขตของเนื้อหา : -
บทคัดย่อ/คำอธิบาย :

Many pathogens, including viruses, bacteria, and protozoan parasites, suppress cellular immune responses through activation of type I IFN signaling. Recent evidence suggests that immune suppression and susceptibility to the malaria parasite, Plasmodium, is mediated by type I IFN; however, it is unclear how type I IFN suppresses immunity to blood-stage Plasmodium parasites. During experimental severe malaria, CD4+ Th cell responses are suppressed, and conventional DC (cDC) function is curtailed through unknown mechanisms. Here, we tested the hypothesis that type I IFN signaling directly impairs cDC function during Plasmodium infection in mice. Using cDC-specific IFNAR1-deficient mice, and mixed BM chimeras, we found that type I IFN signaling directly affects cDC function, limiting the ability of cDCs to prime IFN-γ–producing Th1 cells. Although type I IFN signaling modulated all subsets of splenic cDCs, CD8– cDCs were especially susceptible, exhibiting reduced phagocytic and Th1-promoting properties in response to type I IFNs. Additionally, rapid and systemic IFN-α production in response to Plasmodium infection required type I IFN signaling in cDCs themselves, revealing their contribution to a feed-forward cytokine-signaling loop. Together, these data suggest abrogation of type I IFN signaling in CD8– splenic cDCs as an approach for enhancing Th1 responses against Plasmodium and other type I IFN–inducing pathogens.

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