biostudies-literatureLawrence DWBLRD VAU.S. Department of Veterans Affairse0222802https://www.ebi.ac.uk/biostudies/studies/S-EPMC6754162biostudies-literatureUnknown14(9)Recent studies have begun to elucidate a role for E3 ubiquitin ligases as important mediators of the innate immune response. Our previous work defined a role for the ubiquitin ligase natural killer lytic-associated molecule (NKLAM/RNF19b) in mouse and human innate immunity. Here, we present novel data describing a role for NKLAM in regulating the immune response to Sendai virus (SeV), a murine model of paramyxoviral pneumonia. NKLAM expression was significantly upregulated by SeV infection. SeV-infected mice that are deficient in NKLAM demonstrated significantly less weight loss than wild type mice. In vivo, Sendai virus replication was attenuated in NKLAM-/- mice. Autophagic flux and the expression of autophagy markers LC3 and p62/SQSTM1 were also less in NKLAM-/- mice. Using flow cytometPloS oneMice deficient in NKLAM have attenuated inflammatory cytokine production in a Sendai virus pneumonia model.PMC6754162I01 BX0007051 IO1BX000705Kornbluth JLawrence DWShornick LPfalseMice deficient in NKLAM have attenuated inflammatory cytokine production in a Sendai virus pneumonia model.Recent studies have begun to elucidate a role for E3 ubiquitin ligases as important mediators of the innate immune response. Our previous work defined a role for the ubiquitin ligase natural killer lytic-associated molecule (NKLAM/RNF19b) in mouse and human innate immunity. Here, we present novel data describing a role for NKLAM in regulating the immune response to Sendai virus (SeV), a murine model of paramyxoviral pneumonia. NKLAM expression was significantly upregulated by SeV infection. SeV-infected mice that are deficient in NKLAM demonstrated significantly less weight loss than wild type mice. In vivo, Sendai virus replication was attenuated in NKLAM-/- mice. Autophagic flux and the expression of autophagy markers LC3 and p62/SQSTM1 were also less in NKLAM-/- mice. Using flow cytomet2019-01-01T00:00:00Z20192026-05-06T22:34:43.343Z2019-10-11T07:08:38ZS-EPMC67541623153940010.1371/journal.pone.0222802