Eotaxin-1/CCL11 Is Involved in Cell Migration in Rheumatoid Arthritis

The authors investigated the expression and function of Eotaxin-1 (CCL11) in rheumatoid arthritis fibroblast-like synoviocytes.
[Scientific Reports]
Wakabayashi, K., Isozaki, T., Tsubokura, Y., Fukuse, S., & Kasama, T. (2021). Eotaxin-1/CCL11 is involved in cell migration in rheumatoid arthritis. Scientific Reports, 11(1), 7937. https://doi.org/10.1038/s41598-021-87199-7 Cite
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Does the Epithelial Barrier Hypothesis Explain the Increase in Allergy, Autoimmunity and Other Chronic Conditions?

Scientists discuss how the immune responses to dysbiotic microbiota that cross the damaged barrier may be involved in the development of allergic and autoimmune diseases.
[Nature Reviews Immunology]
Akdis, C. A. (2021). Does the epithelial barrier hypothesis explain the increase in allergy, autoimmunity and other chronic conditions? Nature Reviews Immunology, 1–13. https://doi.org/10.1038/s41577-021-00538-7 Cite
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Sorrento Enters Into Merger Agreement to Acquire Late-Stage Oncology Company ACEA Therapeutics

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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Cellular and Molecular Mechanisms Breaking Immune Tolerance in Inborn Errors of Immunity

Scientists demonstrated that ZIP8 was specifically upregulated in CD4+ T cells that infiltrated the inflamed joint and that ZIP8 deficiency in CD4+ T cells abrogated collagen-induced arthritis.
[Experimental & Molecular Medicine]
Sogkas, G., Atschekzei, F., Adriawan, I. R., Dubrowinskaja, N., Witte, T., & Schmidt, R. E. (2021). Cellular and molecular mechanisms breaking immune tolerance in inborn errors of immunity. Cellular & Molecular Immunology, 1–19. https://doi.org/10.1038/s41423-020-00626-z Cite
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Protectin DX Restores Treg/Th17 Cell Balance in Rheumatoid Arthritis by Inhibiting NLRP3 Inflammasome via miR-20a

Nucleotide-binding domain–like receptor protein 3 (NLRP3) knockout and rescue experiments demonstrated that NLRP3 participated in protectin DX-mediated Treg/Th17 cell balance restoration, joint injury amelioration and inflammatory-response attenuation using Nlrp3−/− mice.
[Cell Death & Disease]
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TNF in the Era of Immune Checkpoint Inhibitors: Friend or Foe?

Data from preclinical studies hint that TNF inhibition might augment the antitumour effect of immune checkpoint inhibitor therapy while simultaneously ameliorating immune-related adverse events.
[Nature Reviews Rheumatology]
Chen, A. Y., Wolchok, J. D., & Bass, A. R. (2021). TNF in the era of immune checkpoint inhibitors: friend or foe? Nature Reviews Rheumatology, 1–11. https://doi.org/10.1038/s41584-021-00584-4 Cite
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Rheumatoid Cachexia: The Underappreciated Role of Myoblast, Macrophage and Fibroblast Interplay in the Skeletal Muscle Niche

The authors summarize the most recent literature characterising clinical rheumatoid arthritis cachexia and links these features to the roles of and complex communication between multiple cellular contributors in the muscle niche, highlighting the importance of a targeted approach to therapeutic intervention.
[Journal of Biomedical Science]
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High miR-451 Expression in Peripheral Blood Mononuclear Cells from Subjects at Risk of Developing Rheumatoid Arthritis

Investigators identified differentially expressed miRNAs in the peripheral blood of ACPA-positive individuals with arthralgia at risk of rheumatoid arthritis compared to healthy controls.
[Scientific Reports]
Prajzlerová, K., Kryštůfková, O., Hánová, P., Horváthová, V., Gregová, M., Pavelka, K., Vencovský, J., Šenolt, L., & Filková, M. (2021). High miR-451 expression in peripheral blood mononuclear cells from subjects at risk of developing rheumatoid arthritis. Scientific Reports, 11(1), 4719. https://doi.org/10.1038/s41598-021-84004-3 Cite
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Jubilant Therapeutics Announces Research Collaboration with Boston Children’s Hospital, Harvard Medical School, to Evaluate PAD4 Inhibitors in Autoimmune/Inflammation Disease Models

Jubilant Therapeutics Inc. announced a collaboration with Boston Children’s Hospital to evaluate peptidyl arginine deiminase 4 (PAD4) inhibitors under development by Jubilant Therapeutics to explore the modulation of neutrophil extracellular traps in preclinical models of neutrophil regulation and rheumatoid arthritis.
[Jubilant Therapeutics Inc.]
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Arachidonic Acid-Regulated Calcium Signaling in T Cells from Patients with Rheumatoid Arthritis Promotes Synovial Inflammation

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.
[Nature Communications]
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
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Location, Location, Location: How the Tissue Microenvironment Affects Inflammation in RA

Emerging evidence indicates an important role for the tissue microenvironment in the pathogenesis of rheumatoid arthritis (RA). Each tissue is made up of cells surrounded and supported by a unique ECM. These complex molecular networks define tissue architecture and provide environmental signals that programme site-specific cell behaviour.
[Nature Reviews Rheumatology]
Buckley, C. D., Ospelt, C., Gay, S., & Midwood, K. S. (2021). Location, location, location: how the tissue microenvironment affects inflammation in RA. Nature Reviews Rheumatology, 1–18. https://doi.org/10.1038/s41584-020-00570-2 Cite
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