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The clinical assessment of lung involvement in patients with Still's disease, results from the multicentre international AIDA Network Still's Disease Registry.

Rheumatology (Oxford)

January 2025

Department of Medical Sciences, Surgery and Neurosciences, Research Center of Systemic Autoinflammatory Diseases and Behçet's Disease Clinic, University of Siena, Siena, Italy.

Objectives: To assess the lung involvement in patients with Still's disease, an inflammatory disease assessing both children and adults. To exploit possible associated factors for parenchymal lung involvement in these patients.

Methods: A multicentre observational study was arranged assessing consecutive patients with Still's disease characterized by the lung involvement among those included in the AIDA (AutoInflammatory Disease Alliance) Network Still's Disease Registry.

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Objective: The mucosal origin hypothesis in rheumatoid arthritis (RA) posits that inhalant exposures, such as cigarette smoke and crystalline silica (c-silica), trigger immune responses contributing to disease onset. Despite the established risk posed by these exposures, the mechanistic link between inhalants, lung inflammation, and inflammatory arthritis remains poorly understood, partly from the lack of a suitable experimental model. As c-silica accelerates autoimmune phenotypes in lupus models and is a recognized risk factor for several autoimmune diseases, we investigated whether c-silica exposure could induce RA-like inflammatory arthritis in mice.

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Systemic lupus erythematosus (SLE) patients are 90% women and over three times more likely to die of cardiovascular disease than women in the general population. Chest pain with no obstructive cardiac disease is associated with coronary microvascular disease (CMD), where narrowing of the small blood vessels can lead to ischemia, and frequently reported by SLE patients. Using whole blood RNA samples, we asked whether gene signatures discriminate SLE patients with coronary microvascular dysfunction (CMD) on cardiac MRI (n = 4) from those without (n = 7) and whether any signaling pathway is linked to the underlying pathobiology of SLE CMD.

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C16 peptide and angiopoietin-1 alleviate the side effects of glucocorticoids in a rat multiple sclerosis model.

Life Sci

January 2025

Institute of Anatomy and Cell Biology, Medical College, Zhejiang University, Hangzhou, China. Electronic address:

Background: Natural glucocorticoids (GCs) have been widely used to treat acute multiple sclerosis (MS) attacks. However, they also cause significant side effects related to immunosuppression. Our previous study found that C16 peptide combined with angiopoietin-1 (Ang-1) inhibited inflammatory cell infiltration and protected blood vessels in animal models of inflammatory neurodegenerative diseases.

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Interferon regulatory factor 5 attenuates kidney fibrosis through transcriptional suppression of Tgfbr1.

Int Immunopharmacol

January 2025

Department of Nephrology, State Key Laboratory of Reproductive Medicine, Children's Hospital of Nanjing Medical University, Nanjing 210008 China; Nanjing Key Laboratory of Pediatrics, Children's Hospital of Nanjing Medical University, Nanjing 210008 China; Jiangsu Key Laboratory of Early Development and Chronic Diseases Prevention in Children, Nanjing Medical University, Nanjing 210029 China. Electronic address:

Tubulointerstitial fibrosis is a common pathway of the progressive development of chronic kidney diseases (CKD) with different etiologies. The transcription factor interferon regulatory factor 5 (IRF5) can induce anti-type I interferons and proinflammatory cytokine genes and has been implicated as a therapeutic target for various inflammatory and autoimmune diseases. Currently, no experimental evidence has confirmed the role of IRF5 in CKD.

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