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| http://dx.doi.org/10.1007/s00277-020-04160-w | DOI Listing |
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A T17-intrinsic IL-1β-STAT5 axis drives steroid resistance in autoimmune neuroinflammation.
Sci Immunol
May 2024
Department of Inflammation and Immunity, Cleveland Clinic Lerner Research Institute, Cleveland, OH, USA.
Steroid resistance poses a major challenge for the management of autoimmune neuroinflammation. T helper 17 (T17) cells are widely implicated in the pathology of steroid resistance; however, the underlying mechanisms are unknown. In this study, we identified that interleukin-1 receptor (IL-1R) blockade rendered experimental autoimmune encephalomyelitis (EAE) mice sensitive to dexamethasone (Dex) treatment.
View Article and Find Full Text PDFIL-1 receptor (IL-1R) signaling can activate thresholded invariant outputs and proportional outputs that scale with the amount of stimulation. Both responses require the Myddosome, a multiprotein complex. The Myddosome is required for polyubiquitin chain formation and NF-kB signaling.
View Article and Find Full Text PDFSynovial macrophages of rheumatoid arthritic mice protectively responded by altered M1/M2 differentiation after antibody blocking of TNFR1 and IL-1R.
Int Immunopharmacol
February 2023
Department of Physiology, Immunology Laboratory, University of Calcutta, University Colleges of Science and Technology, 92 APC Road, Calcutta 700009, West Bengal, India. Electronic address:
Rheumatoid arthritis (RA) primarily affecting the synovial tissue, has emerged as a major concern leading to the pressing need to develop effective treatment strategies. In the affected synovial tissue, resident macrophages play a pivotal role in the pathogenesis of RA. TNF-α and IL-1β released from pro-inflammatory M1 synovial macrophages are the master regulators of chronic joint inflammation.
View Article and Find Full Text PDFIL-1β is not critical to chronic heart dysfunction in mice with Chagas disease.
Front Immunol
November 2022
Institute of Biophysics Carlos Chagas Filho, Federal University of Rio de Janeiro (UFRJ), Rio de Janeiro, Brazil.
Long after infection, 40% of individuals develop a progressive chronic chagasic cardiomyopathy (CCC), with systolic dysfunction and arrhythmias. Since we previously showed IL-1β mediates the development of systolic dysfunction and cardiac arrhythmias in diabetes mellitus and cardiorenal syndrome, and IL-1β remains elevated in Chagas disease patients, here we tested the role of IL-1β in CCC using a mouse model. Mice deficient in IL-1R expression ( ) survived acute infection with greater parasitemia than controls but did not lose weight as wild-type (WT) did.
View Article and Find Full Text PDFIL-1β-dependent extravasation of preexisting lung-restricted autoantibodies during lung transplantation activates complement and mediates primary graft dysfunction.
J Clin Invest
October 2022
Division of Thoracic Surgery.
Preexisting lung-restricted autoantibodies (LRAs) are associated with a higher incidence of primary graft dysfunction (PGD), although it remains unclear whether LRAs can drive its pathogenesis. In syngeneic murine left lung transplant recipients, preexisting LRAs worsened graft dysfunction, which was evident by impaired gas exchange, increased pulmonary edema, and activation of damage-associated pathways in lung epithelial cells. LRA-mediated injury was distinct from ischemia-reperfusion injury since deletion of donor nonclassical monocytes and host neutrophils could not prevent graft dysfunction in LRA-pretreated recipients.
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