interferon and immune responses

This study shows that cGAS-STING-dependent type I IFN signaling is required for host defense against Leptospira interrogans in mice by reducing renal colonization.

The study shows that SARS-CoV-2 nucleocapsid protein persistence without viral replication leads to type I interferon production and mitochondrial dysfunction, promoting autoimmunity.

This study identifies RNA-binding proteins regulated by type I IFN, revealing a new layer of antiviral response involving post-translational regulation of RNA binding.

The paper identifies genetic variants that influence neuronal responses to interferons by analyzing gene expression and STAT1 binding in iPSC-derived neurons.

This paper shows that STAT5A deficiency disrupts actin networks, leading to mitochondrial dysfunction and IFN-beta production, which can be reversed by restoring ACTN1.

The paper develops a mathematical model to show how NFκB and IRF-3 co-regulate IFNβ expression during viral infections, with NFκB driving immediate response and IRF-3 causing delayed but persistent expression.

This study shows that CGAS and STING1 genes are pseudogenized in armadillos, suggesting alternative mechanisms for sensing dsDNA and possibly contributing to their cancer resistance.

This study shows FMDV infection in horse cells increases lactate, which modifies VDAC1 and promotes mtDNA release, activating cGAS-STING and reducing viral replication.

This paper develops a ratio-based biomarker (DIRECT LS-TA) using monocyte-specific gene expression ratios in peripheral blood to improve viral infection triage, outperforming the IFN score in diagnostic accuracy.

This study shows that NOD2 promotes coxsackievirus B3 replication in intestinal epithelial cells by suppressing Type 1 Interferon expression and MDA5 activation through NOD2-mediated mitophagy.

This study identifies ISG15 as a key host defense mechanism against Salmonella typhoid toxin, showing it promotes cell survival and reduces bacterial burden through a STING-dependent pathway.

This study identifies MAVS as a mitochondrial guardian that maintains mitochondrial integrity to drive IFN-independent antiviral immunity against SARS-CoV-2 and JEV.

The paper reveals how ALT+ cells sustain cGAS-STING activation through spatial regulation and lysosomal degradation of STING and ECTR species, suggesting therapeutic targets for ALT+ tumors.

This study identifies DCA as a microbiota-derived bile acid that activates STING and enhances antitumor immunity via NK cell activation.

The paper develops a NanoBRET assay to monitor USP18 interactions and identifies a small molecule inhibitor of USP18/ISG15 binding.

This paper shows that inhibiting interferon signaling enhances RHDV replication in rabbit liver organoids, enabling serial passaging for the first time.

This paper describes the development of SB 11285, a potent and bioavailable STING agonist showing antitumor activity in mouse models and undergoing clinical trials for cancer immunotherapy.

This study shows Huwe1 is essential for RIG-I-like receptor-mediated type I and III IFN induction by ubiquitinating key pathway components like TRAF5.

The paper identifies mechanisms that prevent innate immune activation by TE-derived cytosolic DNA, preserving pluripotency in ESCs.

This study identifies UFMylation sites on 14-3-3ϵ that regulate MAVS complex assembly and RIG-I signaling to enhance antiviral innate immunity.

The paper identifies intrinsic OASL expression as a determinant of IFN induction potential in influenza A virus-infected cells using scRNA-seq analysis.

The paper shows that pluripotent mouse embryonic stem cells silence MDA5 to avoid endogenous dsRNA recognition, preventing IFN activation and ensuring normal development.

The paper investigates the structural interaction between HAQ STING and COPA, identifying a potential drug-binding pocket that could lead to therapeutic strategies for COPA disease.

The paper identifies a regulatory mechanism that tunes cGAS signaling by cleaving a catalytic intermediate, preventing excessive activation while preserving immune function.

This study shows caspase-3 cleaves activated MAVS to suppress spontaneous innate immune signaling in non-apoptotic cells.

This study identifies two novel cis-regulatory elements and IRF1 as a regulator of NLRC5, revealing how viral factors inhibit IFNγ-mediated MHC class I pathway.

This study demonstrates that enterovirus 2A protease is critical for viral replication and evasion of host antiviral responses through multiple mechanisms.

This study identifies a mechanism where AMPK and cGAS-STING signaling synergize through glucose and dsDNA sensing to enhance antitumor immunity in melanoma and colorectal cancer.

The paper shows that short 5' UTRs in viral mRNAs are recognized by the IFIT2-IFIT3 complex, leading to translation inhibition and antiviral activity.