Superficial Immunity: Antimicrobial Responses Are More Than Skin Deep

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Presentation transcript:

Superficial Immunity: Antimicrobial Responses Are More Than Skin Deep Madison R. Mack, Brian S. Kim Immunity Volume 45, Issue 1, Pages 6-8 (July 2016) DOI: 10.1016/j.immuni.2016.07.001 Copyright © 2016 Elsevier Inc. Terms and Conditions

Figure 1 Keratinocytes Amplify IFN-β Production in Response to LL37 and dsRNA Released from Damaged Skin LL37 and dsRNA are released from damaged keratinocytes during wounding and in psoriasis lesions. dsRNA is detected by cytosolic sensors, which together with LL37 signal through MAVS to produce phosphorylated IRF3. Phosphorylated IRF3 can then initiate transcription of IFNB1 in keratinocytes, which in turn activates cDCs to promote inflammation. In psoriasis, cDCs recruit Th17 cells to drive disease pathogenesis. In addition to the role of LL37 in mediating direct antibacterial defense, it provides antiviral activity via regulation of IFN-β. IFN, interferon; dsRNA, double-stranded RNA; MAVS, mitochondrial antiviral signaling protein; IRF3, interferon regulatory factor 3; cDC, conventional dendritic cell; Th17, T helper type 17. Immunity 2016 45, 6-8DOI: (10.1016/j.immuni.2016.07.001) Copyright © 2016 Elsevier Inc. Terms and Conditions