MSCs-Released TGFβ1 Generate CD4+CD25+Foxp3+ in T-Reg Cells of Human SLE PBMC

The authors used a post-test control group design. MSCs were obtained from human umbilical cord blood and characterized according to their surface antigen expression and multilineage differentiation capacities.
[Journal of the Formosan Medical Association]
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Emerging Evidence of a COVID-19 Thrombotic Syndrome Has Treatment Implications

Reports of widespread thromboses and disseminated intravascular coagulation in patients with coronavirus disease 19 (COVID-19) have been rapidly increasing in number. This perspective has critical implications for treatment.
[Nature Reviews Rheumatology]
Merrill, J. T., Erkan, D., Winakur, J., & James, J. A. (2020). Emerging evidence of a COVID-19 thrombotic syndrome has treatment implications. Nature Reviews Rheumatology, 1–9. https://doi.org/10.1038/s41584-020-0474-5 Cite
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Aurinia Announces US Food and Drug Administration Acceptance of the Filing of New Drug Application and Priority Review for Voclosporin for the Treatment of Lupus Nephritis

Aurinia Pharmaceuticals, Inc. announced that the US FDA has accepted the filing of its New Drug Application for voclosporin, as a potential treatment for lupus nephritis, a serious inflammation of the kidneys caused by the autoimmune disease systemic lupus erythematosus.

Aurinia Pharmaceuticals, Inc.]

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Feinstein Institutes Receives $15 Million NIH Grant to Study Brain Dysfunction in Lupus

The Feinstein Institutes for Medical Research has been awarded a $15 million grant to study brain dysfunction tied to lupus by the National Institutes of Health. Betty Diamond, MD, director of the Feinstein’s Institute of Molecular Medicine, will use the five-year grant to investigate the role of anti-N-methyl D-aspartate receptor.
[The Feinstein Institutes for Medical Research (Business Wire, Inc.)]
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Macrophage Metabolic Reprogramming Presents a Therapeutic Target in Lupus Nephritis

Investigators found that human and mouse macrophages underwent a switch to glycolysis in response to IgG immune complex stimulation, mirroring macrophage metabolic changes in inflamed tissue in vivo. This metabolic reprogramming was required to generate a number of proinflammatory mediators, including IL-1β, and was dependent on mTOR and hypoxia-inducible factor-1α.
[Proceedings of the National Academy of Sciences of the United States of America]
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