Mechanistic considerations linking SARS-CoV-2 infection, inflammation, and the loss of immune tolerance DOI Creative Commons
Antonio Tonutti, Francesca Motta, Natasa Isailovic

et al.

Current Opinion in Immunology, Journal Year: 2025, Volume and Issue: 95, P. 102567 - 102567

Published: May 23, 2025

The immune response to SARS-CoV-2 has been implicated in the onset of multiple, seemingly unrelated, autoimmune diseases. also unmasking and/or production multiple autoantibodies, even absence clinical disease. Despite such data, it remains unclear whether antibodies targeting antiviral signaling proteins and mitochondrial antigens reflect bystander activation or alternatively contribute de novo viral escape mechanisms. With these comments mind, a variety professional antibody presenting cells including lung resident macrophages COVID-19 infected patients are impacted dependent on uptake antibody-opsonized virus by Fcγ receptors; yet infection is aborted via antibody-dependent effector mechanisms pyroptosis, possibly leading autoantibody production, autoinflammatory manifestations, respectively. TRIM21/Ro52, cytosolic E3-ubiquitin ligase with an Fc-gamma receptor domain, functions as intracytoplasmic receptor, directs complexes binding virions but autoantigens autophagy. During autophagy, Ig-virions-TRIM21/Ro52-autoantigens bind directly class II human leukocyte antigen lysosomal compartment, subsequent presentation cell surface. This process favors development specific humoral potential lead loss tolerance. Interestingly, TRIM21/Ro52 can pyroptosis. We propose that well-placed at crossroad between inflammatory autoimmunity.

Language: Английский

Mechanistic considerations linking SARS-CoV-2 infection, inflammation, and the loss of immune tolerance DOI Creative Commons
Antonio Tonutti, Francesca Motta, Natasa Isailovic

et al.

Current Opinion in Immunology, Journal Year: 2025, Volume and Issue: 95, P. 102567 - 102567

Published: May 23, 2025

The immune response to SARS-CoV-2 has been implicated in the onset of multiple, seemingly unrelated, autoimmune diseases. also unmasking and/or production multiple autoantibodies, even absence clinical disease. Despite such data, it remains unclear whether antibodies targeting antiviral signaling proteins and mitochondrial antigens reflect bystander activation or alternatively contribute de novo viral escape mechanisms. With these comments mind, a variety professional antibody presenting cells including lung resident macrophages COVID-19 infected patients are impacted dependent on uptake antibody-opsonized virus by Fcγ receptors; yet infection is aborted via antibody-dependent effector mechanisms pyroptosis, possibly leading autoantibody production, autoinflammatory manifestations, respectively. TRIM21/Ro52, cytosolic E3-ubiquitin ligase with an Fc-gamma receptor domain, functions as intracytoplasmic receptor, directs complexes binding virions but autoantigens autophagy. During autophagy, Ig-virions-TRIM21/Ro52-autoantigens bind directly class II human leukocyte antigen lysosomal compartment, subsequent presentation cell surface. This process favors development specific humoral potential lead loss tolerance. Interestingly, TRIM21/Ro52 can pyroptosis. We propose that well-placed at crossroad between inflammatory autoimmunity.

Language: Английский

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