Journal
JOURNAL OF AUTOIMMUNITY
Volume 130, Issue -, Pages -Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.jaut.2022.102840
Keywords
RIG-I; Nuclear localization; Cellular apoptosis; Viral infection; Systemic lupus erythematosus
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Funding
- National Natural Sci-ence Foundation of China [81788101and 82171726]
- CAMS Inno-vation Fund for Medical Sciences [2021-I2M-1-017]
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This study reveals a non-canonical role of nuclear RIG-I in the induction of cellular apoptosis, besides its activation of IFN-I expression as the cytosolic innate sensor. The interaction between nuclear RIG-I and APEX1 provides new insight into the regulation of infection, IFN-I, and autoimmune diseases.
Cell death is important in the elimination of damaged cells such as virus-infected cells and also is closely involved in the pathogenesis of autoimmune diseases such as systemic lupus erythematosus (SLE). The retinoic acidinducible gene-I (RIG-I), one cytosolic RNA innate sensor, can trigger antiviral innate response by inducing production of type I interferons (IFN-I). However, the function of RIG-I, once translocated from cytoplasm to nucleus at the late stage of viral infection when IFN-I production is almost terminated, remains poorly understood. Here, we reported that RIG-I is accumulated in the nucleus of macrophages and fibroblasts after virus infection, and nuclear RIG-I is present in peripheral blood mononuclear cells (PBMCs) from SLE patients. We found that nuclear RIG-I interacts with the first 20 amino acids of apurinic/apyrimidinic endodeoxyribonuclease 1 (APEX1) and attenuates the anti-apoptotic properties of APEX1, therefore promoting apoptosis of virus-infected cells to suppress viral infection through an IFN-I-independent way at the late stage of viral infection. Together, our findings reveal a non-canonical role of nuclear RIG-I in the induction of cellular apoptosis, besides its activation of IFN-I expression as the cytosolic innate sensor. This study provides new insight to the regulation of infection, IFN-I and autoimmune diseases by nuclear RIG-I-APEX1 interaction.
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