NK cell activation provides protection against herpes simplex encephalitis through TLR3/TRIF-dependent crosstalk between epithelial and dendritic cells

Abstract Herpes simplex encephalitis (HSE), which is a fatal disease causing focal or global cerebral dysfunction following infection with herpes virus type 1 (HSV-1). Previous few studies have been administered on the immunopathological networks of HSE in context TLR3 and TRIF defects at cellular molecular levels. In this work, we tried to decipher crosstalk between I IFN (IFN-I)-producing epithelial layer IL-15-producing dendritic cells (DC) activate NK for protective role TLR3/TRIF pathway progression after vaginal HSV-1 infection. TLR3- TRIF-knockout mice showed enhanced susceptibility progression, high burden tract, lymphoid system, CNS. The increased TRIF-ablated did not correlate infiltration Ly-6C +monocytes, but it was closely associated impaired cell activation tract. addition, using delicate ex vivo experiments bone marrow transplantation, deficiency tissue-resident cells, such as found cause by means low IFN-I production, whereas receptor DC play activating via IL-15 production response produced from layer. These results provide new information about IFN-I- IL-15-mediated primary site that can suppress TRIF-dependent manner. This study supported Basic Science Research Program through National Foundation Korea (NRF) grants funded Ministry Education ICT (MSIT), Republic (2021R1A2B5B02001578, 2019R1A6A1A03033084 Seong Kug Eo, 2020R1I1A1A01054533 Erdenebileg Uyangaa, 2020R1I1A2055591 Jin Young Choi, http://www.nrf.re.kr).