Given the known involvement of IL-36 in psoriasis it might be surprising that the latest mouse models show that inhibiting IL-36 signalling does not alter the course of inflammatory arthritis. Can we now add IL-36 to the list of inflammatory mediators that are not viable DMARD targets?
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http://dx.doi.org/10.1038/nrrheum.2014.156 | DOI Listing |
Cell Commun Signal
January 2025
Division of Rheumatology, Department of Medicine, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
Background: Interleukin (IL)-38 is an IL-1 family cytokine that was proposed to exert anti-inflammatory effects. However, its mechanisms of action are not well understood and the identity of the IL-38 receptor(s) remains debated. Proposed candidates include the IL-1 receptor (IL-1R1), the IL-36 receptor (IL-36R) and the orphan receptor IL-1RAPL1.
View Article and Find Full Text PDFHum Immunol
January 2025
Department of Rheumatology, Faculty of Medicine, Firat University, Elazig, Turkey.
Background: Idiopathic granulomatous mastitis (IGM) is a chronic inflammatory disorder characterised by the formation of non-caseating granulomas in breast tissue, primarily affecting young women of childbearing age. The aetiology of IGM remains unclear, with potential factors including trauma, hormonal influences, and autoimmune responses. Recent studies suggest that immune dysregulation may play a critical role in IGM, highlighting the need for exploration of biomarkers involved in inflammation and immune modulation, particularly LL-37, galectin-3, IL-36, and TLR3.
View Article and Find Full Text PDFFront Immunol
November 2024
Rheumatology, Shanghai Jiao Tong University School of Medicine Affiliated Renji Hospital, Shanghai, China.
Antibody drugs targeting single inflammatory cytokines have revolutionized the treatment of immune-mediated inflammatory diseases. To investigate whether dual targeting interleukin-17 (IL-17) and IL-36 enhances anti-inflammatory activity, bispecific Ab HB0043 was generated by linking the single chain fragment variables (scFvs) from humanized anti-IL-36R antibody (HB0034) to the C-terminus of the heavy chain of anti-IL-17A IgG1 (HB0017) Fc using a flexible peptide linker. HB0043 largely maintained the binding affinities and biological activities of the two parent monoclonal antibodies (mAbs) .
View Article and Find Full Text PDFCirc Heart Fail
December 2024
Department of Pathology, School of Medicine (D.A.L., D.E., M.V.T., D.Č.), Johns Hopkins University, Baltimore, MD.
Background: Currently, there are no therapies targeting specific pathogenic pathways in myocarditis. IL (interleukin)-1 blockade has shown promise in preclinical studies and case reports. We hypothesized that blockade of IL1RAP (IL-1 receptor accessory protein), a shared subunit of the IL-1, IL-33, and IL-36 receptors, could be more efficient than IL-1 blockade alone.
View Article and Find Full Text PDFJ Dermatol
January 2025
Department of Dermatology, Kansai Medical University, Osaka, Japan.
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