ArticlePloS one2015
Infection of Female BWF1 Lupus Mice with Malaria Parasite Attenuates B Cell Autoreactivity by Modulating the CXCL12/CXCR4 Axis and Its Downstream Signals PI3K/AKT, NFκB and ERK.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 32 citations in OpenAlex.
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- Dual nature of type I interferon responses and feedback regulations by SOCS1 dictate malaria mortality.Journal of advanced research · 2025Article
- The regulatory functions of G protein-coupled receptors signaling pathways in B cell differentiation and development contributing to autoimmune diseases.Cell & bioscience · 2025Review
- The story of clobenpropit and CXCR4: can be an effective drug in cancer and autoimmune diseases?Frontiers in pharmacology · 2024Review
- CCL17-producing cDC2s are essential in end-stage lupus nephritis and averted by a parasitic infection.The Journal of clinical investigation · 2021Article
- The Role of CXCL12 in Kidney Diseases: A Friend or Foe?Kidney diseases (Basel, Switzerland) · 2021Review
- Microarray expression and functional analysis of circular RNAs in the glomeruli of NZB/W F1 mice with lupus nephritis.Experimental and therapeutic medicine · 2019Article
- The Role of the CXCL12/CXCR4/ACKR3 Axis in Autoimmune Diseases.Frontiers in endocrinology · 2019Review
- Clinical characteristics and risk factors of infections in patients with systemic lupus erythematosus.Clinical rheumatology · 2018Article
- Contribution and underlying mechanisms of CXCR4 overexpression in patients with systemic lupus erythematosus.Cellular & molecular immunology · 2017Article
- SDF1-CXCR4 Signaling Contributes to the Transition from Acute to Chronic Pain State.Molecular neurobiology · 2017Article
- Infection in systemic lupus erythematosus, similarities, and differences with lupus flare.The Korean journal of internal medicine · 2017Review
- Parasite-Derived Proteins for the Treatment of Allergies and Autoimmune Diseases.Frontiers in microbiology · 2017Review
- Chemokines and Chemokine Receptors in the Development of Lupus Nephritis.Mediators of inflammation · 2016Review
- Methylprednisolone attenuates lipopolysaccharide-induced Fractalkine expression in kidney of Lupus-prone MRL/lpr mice through the NF-kappaB pathway.BMC nephrology · 2015Article
- High-Salt Enhances the Inflammatory Response by Retina Pigment Epithelium Cells following Lipopolysaccharide Stimulation.Mediators of inflammation · 2015Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterized by abnormal autoreactivity in B cells. Lymphocytes and their soluble mediators contribute to the disease pathogenesis. We recently demonstrated that infecting lupus mice with malaria confers protection against lupus nephritis by attenuating oxidative stress in both liver and kidney tissues. In the current study, we further investigated B cell autoreactivity in female BWF1 lupus mice after infection with either live or gamma-irradiated malaria, using ELISA, flow cytometry and Western blot analysis. The lupus mice exhibited a significant elevation in plasma levels of IL-4, IL-6, IL-7, IL-12, IL-17, IFN-α, IFN-γ, TGF-β, BAFF and APRIL and a marked elevation of IgG2a, IgG3 and ant-dsDNA autoantibodies compared with normal healthy mice. Infecting lupus mice with live but not gamma-irradiated malaria parasite partially and significantly restored the levels of the soluble mediators that contribute to the progression of lupus. Furthermore, the B cells of lupus mice exhibited an increased proliferative capacity; aberrant overexpression of the chemokine receptor CXCR4; and a marked elevation in responsiveness to their cognate ligand (CXCL12) via aberrant activation of the PI3K/AKT, NFκB and ERK signaling pathways. Interestingly, infecting lupus mice with live but not gamma-irradiated malaria parasite restored a normal proliferative capacity, surface expression of CXCR4 and B cell response to CXCL-12. Taken together, our data present interesting findings that clarify, for the first time, the molecular mechanisms of how infection of lupus mice with malaria parasite controls B cell autoreactivity and thus confers protection against lupus severity.
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