ArticleThe Journal of biological chemistry2013
DNA-dependent activator of interferon-regulatory factors (DAI) promotes lupus nephritis by activating the calcium pathway.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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35 citing papers in PubMed, 72 citations in OpenAlex.
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- Activation of Innate Immunity by Therapeutic Nucleic Acids.International journal of molecular sciences · 2021Review
- Azithromycin alleviates systemic lupus erythematosus via the promotion of M2 polarisation in lupus mice.Cell death discovery · 2021Article
- Extracellular Fragmented Self-DNA Is Involved in Plant Responses to Biotic Stress.Frontiers in plant science · 2021Article
- STING, the Endoplasmic Reticulum, and Mitochondria: Is Three a Crowd or a Conversation?Frontiers in immunology · 2020Review
- M2b macrophage polarization and its roles in diseases.Journal of leukocyte biology · 2019Review
- Extracellular Chromatin Triggers Release of Soluble CEACAM8 Upon Activation of Neutrophils.Frontiers in immunology · 2019Article
- Changes of NADH Fluorescence from the Skin of Patients with Systemic Lupus Erythematosus.BioMed research international · 2019Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMacrophage M2b polarization conferred by self-DNA immunization initiates and propagates lupus nephritis.
resultsKnockdown of DNA-dependent activator of interferon-regulatory factors (DAI) ameliorates SLE syndrome via blunting macrophage M2b polarization.
conclusionDAI functions as a DNA sensor in self-DNA-induced macrophage M2b polarization and lupus nephritis. SIGNIFICANCE: We disclose the mechanism by which self-DNA induces macrophage M2b polarization and lupus nephritis DNA-dependent activator of interferon-regulatory factors (DAI) functions as a cytoplasmic DNA sensor that activates the innate immune system. We previously found that activated lymphocyte-derived self-apoptotic DNA (ALD-DNA) immunization led to pathological macrophage activation and M2b polarization, which could initiate and propagate murine lupus nephritis. However, the specific DNA sensor(s) as well as underlying molecular mechanisms involved in ALD-DNA-induced macrophage M2b polarization in systemic lupus erythematosus (SLE) disease remains unknown. In this study, we reported that DAI expression was significantly increased in SLE patients as well as in lupus mice. Gain- and loss-of-function studies revealed that DAI was involved in ALD-DNA-induced macrophage activation and M2b polarization. Moreover, ALD-DNA notably induced dimerization/oligomerization of DAI and consequently activation of nuclear factor κB (NF-κB) and interferon regulatory factor 3 (IRF3) signaling pathways via calcium signaling, resulting in macrophage activation and M2b polarization. More importantly, blockade of DAI in vivo or selective knockdown of DAI in macrophages could ameliorate SLE syndrome via blunting macrophage M2b polarization and inhibiting inflammatory response in lupus mice. Our results suggest that DAI could function as a DNA sensor and a regulator in ALD-DNA-induced macrophage M2b polarization and lupus nephritis, providing the possible molecular mechanisms involved in ALD-DNA-induced macrophage M2b polarization in SLE disease and making DAI as a potential therapeutic target for the treatment of SLE.
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