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Articles by Eric Bartnicki
Type 2 immune history trains lung macrophages for viral disease tolerance
Abstract Severe respiratory viral disease varies widely among individuals and often reflects immunopathology rather than inadequate pathogen control, suggesting that previous immune history can prime the lungs towards disease tolerance. Here we show that nerve- and airway-associated macrophages (NAMs), a subset of interstitial macrophages, expand ephemerally after type 2 inflammation induced by Nippostrongylus brasiliensis.
Nerve- and airway-associated interstitial macrophages mitigate SARS-CoV-2 pathogenesis via type I interferon signaling
Keywords tissue-resident macrophages SARS-CoV-2 MA-10 Siglec-1 CD169 nerve- and airway-associated interstitial macrophages innate immunity disease tolerance immunoregulation interferons immunosuppression Get full text access Log in, subscribe or purchase for full access. References 1. Wei, X. ∙ Narasimhan, H. ∙ Zhu, B. ... Host Recovery from Respiratory Viral Infection Annu. Rev. Immunol. 2023; 41:277-300 2. Aegerter, H.
MAVS Signaling Is Required for Preventing Persistent Chikungunya Heart Infection and Chronic Vascular Tissue Inflammation
Abstract Chikungunya virus (CHIKV) infection has been associated with severe cardiac manifestations, yet, how CHIKV infection leads to heart disease remains unknown. Here, we leveraged both mouse models and human primary cardiac cells to define the mechanisms of CHIKV heart infection. Using an immunocompetent mouse model of CHIKV infection as well as human primary cardiac cells, we demonstrate that CHIKV directly infects and actively replicates in cardiac fibroblasts.
KEAP1 mutation in lung adenocarcinoma promotes immune evasion and immunotherapy resistance
Highlights • KEAP1 mutations in lung cancer suppress anti-tumor CD103 DC and CD8 T cell responses • Hyperactivation of NRF2 is responsible for immune evasion in KEAP1-mutant tumors • Glutaminase inhibition can sensitize KEAP1-mutant tumors to immunotherapy Summary Lung cancer treatment has benefited greatly through advancements in immunotherapies. However, immunotherapy often fails in patients with specific mutations like KEAP1, which are frequently found in lung adenocarcinoma.
MAVS signaling is required for preventing persistent chikungunya heart infection and chronic vascular tissue inflammation - Nature Communications
Abstract Chikungunya virus (CHIKV) infection has been associated with severe cardiac manifestations, yet, how CHIKV infection leads to heart disease remains unknown. Here, we leveraged both mouse models and human primary cardiac cells to define the mechanisms of CHIKV heart infection. Using an immunocompetent mouse model of CHIKV infection as well as human primary cardiac cells, we demonstrate that CHIKV directly infects and actively replicates in cardiac fibroblasts.
MAVS signaling is required for clearance of chikungunya heart infection and prevention of chronic inflammation in vascular tissue
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