Sorrento Therapeutics, Inc. announced the signing of a merger agreement pursuant to which Sorrento will acquire ACEA Therapeutics, Inc. The acquisition will include late clinical stage drug Abivertinib, clinical stage candidate AC0058, preclinical stage candidate AC0939, and ACEA’s extensive proprietary library of small molecules, which potentially have applications for numerous human disease indications, including non-small cell lung cancer, B cell lymphomas, systemic lupus, rheumatoid arthritis, multiple sclerosis and viral infections.
[Sorrento Therapeutics, Inc. (Globe Newswire, Inc.)]
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Scientists showed downregulation of mitochondria-derived genes and mitochondria-associated metabolic pathways in IFN-High patients from transcriptomic analysis of CD4+ and CD8+ T cells.
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Buang, N., Tapeng, L., Gray, V., Sardini, A., Whilding, C., Lightstone, L., Cairns, T. D., Pickering, M. C., Behmoaras, J., Ling, G. S., & Botto, M. (2021). Type I interferons affect the metabolic fitness of CD8 + T cells from patients with systemic lupus erythematosus. Nature Communications, 12(1), 1980. https://doi.org/10.1038/s41467-021-22312-y Cite
Using Fas deficient, MRL/MpJ-Faslpr/J mice, which develop lupus-like disease spontaneously, investigators tested the hypothesis that a peptide mimic of the suppressor of cytokine signaling-1 kinase inhibitory region would inhibit lymphocyte activation and modulate lupus-associated pathologies.
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Investigators showed XIST was continually required in adult human B cells to silence a subset of X-linked immune genes such as TLR7.
Researchers discuss the latest discoveries in molecular biology, a platform model of pluripotent stem cells in the SARS-CoV-2 study on 3D animal models and nanoconjugates based on stem cells.
[Stem Cell Research]
Investigators showed that CD4+ T cells from patients with rheumatoid arthritis and psoriatic arthritis had increased expression of the pore-forming calcium channel component ORAI3.
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Ye, Z., Shen, Y., Jin, K., Qiu, J., Hu, B., Jadhav, R. R., Sheth, K., Weyand, C. M., & Goronzy, J. J. (2021). Arachidonic acid-regulated calcium signaling in T cells from patients with rheumatoid arthritis promotes synovial inflammation. Nature Communications, 12(1), 907. https://doi.org/10.1038/s41467-021-21242-z Cite
Scientists observed that αVβ6 could mediate TGF-β1 bioavailability and that VTN(381–397 A.A.) could prevent TGF-β1 activation by interacting with αVβ6 in human fibroblast-like synoviocytes and increased α-SMA.
[Experimental and Molecular Medicine]
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Ciregia, F., Deroyer, C., Cobraiville, G., Plener, Z., Malaise, O., Gillet, P., Fillet, M., Malaise, M. G., & de Seny, D. (2021). Modulation of α V β 6 integrin in osteoarthritis-related synovitis and the interaction with VTN (381–397 a.a.) competing for TGF-β1 activation. Experimental & Molecular Medicine, 1–13. https://doi.org/10.1038/s12276-021-00558-2 Cite
MRL/lpr mice were injected with miR-199a-5p agomir to evaluate the effects of miR-199a-5p on splenic CD4+ T cell senescence and disease in vivo.
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The authors update our understanding of B cell biology, review the results of clinical trials using B cell depletion therapies (BCDT) in autoimmune indications, discuss hypotheses for the mechanism of action of BCDT and speculate on evolving strategies for targeting B cells beyond depletion.
[Nature Reviews Drug Discovery]
The authors describe two aspects of the clinical therapeutic effects of human umbilical cord (hUCs)-MSCs. They explains the benefits and mechanisms of HUC-MSC treatment in various diseases.
[Stem Cell Research & Therapy]
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The authors showed that in preclinical autoimmunity and established systemic lupus erythematosus, plasmacytoid dendritic cells were not effector cells, had lost capacity for Toll-like-receptor-mediated cytokine production and did not induce T cell activation.
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Psarras, A., Alase, A., Antanaviciute, A., Carr, I. M., Md Yusof, M. Y., Wittmann, M., Emery, P., Tsokos, G. C., & Vital, E. M. (2020). Functionally impaired plasmacytoid dendritic cells and non-haematopoietic sources of type I interferon characterize human autoimmunity. Nature Communications, 11(1), 6149. https://doi.org/10.1038/s41467-020-19918-z Cite