Language：English  

DOI： 10.1093/mrcr/rxag023

PubMed

Language：English   Publisher：Arthritis Research and Therapy  

Background: The efficacy of rituximab (RTX) for the treatment of systemic sclerosis-associated interstitial lung disease (SSc-ILD) has not been fully established. This study compared the efficacy and safety of RTX and intravenous cyclophosphamide (CY) for SSc-ILD. Methods: This retrospective study compared the efficacy and safety of RTX (20 patients) and CY (30 patients) after adjusting for the stabilised inverse probability of treatment weighting based on propensity scores. The efficacy endpoints were the absolute changes in forced vital capacity (FVC) and serum Krebs von den Lungen-6 (KL-6) levels from baseline to 6 and 12 months after treatment. The incidence of progression based on the definition of progressive pulmonary fibrosis was also recorded. The safety endpoint was the frequency of adverse events. Results: The clinical characteristics of the two groups were well-balanced after adjusting for confounders (i.e., FVC, nintedanib use, and newly diagnosed cases). From baseline to 6 and 12 months after the start of treatment, the median FVC increased by 50 and 60 ml in the RTX group and 40 and 15 ml in the CY group, respectively, with no difference after adjustment. The changes in serum KL-6 levels and the incidences of progression were identical in both groups after adjustment. The overall adverse events were similar in both groups after adjustment. Conclusions: RTX demonstrated comparable safety and efficacy as CY in patients with SSc-ILD. Thus, RTX may be an alternative to CY for the treatment of SSc-ILD.

DOI： 10.1186/s13075-025-03654-0

Web of Science

Scopus

PubMed

Language：English   Publisher：Journal of Clinical Medicine  

Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by a multistep pathogenesis, from the preclinical phase of autoantibody emergence to the clinical onset of synovitis and joint destruction. Cytokines play central roles throughout this progression by orchestrating immune cell activation, tissue inflammation, and bone erosion. In the preclinical phase, several cytokines, including IL-12, IL-6, IL-21 and TGF-β, promote Tfh and Tph cell differentiation, helping autoreactive B cells to produce ACPA. During the clinical phase, TNF-α, IL-6, and IL-1β drive synovitis by activating macrophages and fibroblast-like synoviocytes, while also promoting RANKL (Receptor Activator of Nuclear factor κB Ligand) expression and osteoclast differentiation. This review highlights the pathogenic role of cytokines in RA and discusses their relevance as biomarkers and therapeutic targets. A better understanding of cytokine networks may offer new opportunities for early intervention and disease prevention in RA.

DOI： 10.3390/jcm14186409

Web of Science

Scopus

PubMed

Authorship：Lead author   Language：English   Publisher：Modern Rheumatology Case Reports  

A 53-year-old man with adult-onset Still’s disease developed severe streptococcal toxic shock syndrome (STSS) due to Streptococcus dysgalactiae subsp. equisimilis (SDSE), following retroperitoneal panniculitis. He was receiving tocilizumab (TCZ), an interleukin-6 receptor inhibitor. The modifying effect of TCZ on the immune response and the pathophysiology of SDSE infection may have led to retroperitoneal panniculitis and atypical STSS with delayed shock and flare of soft tissue inflammation.

DOI： 10.1093/mrcr/rxae001

Web of Science

Scopus

PubMed

Language：English   Publisher：Rheumatology (United Kingdom)  

Objectives: Recently, the involvement of basophils and IgE-type autoantibodies in the pathogenesis of SLE has been elucidated using mouse models; however, few studies have been conducted in humans. In this study, the role of basophils and anti-double-stranded DNA (dsDNA) IgE in SLE was examined using human samples. Methods: The correlation between disease activity and serum levels of anti-dsDNA IgE in SLE was evaluated using enzyme-linked immunosorbent assay. Cytokines produced by IgE-stimulated basophils from healthy subjects were assessed using RNA sequences. The interaction of basophils and B cells to promote B cell differentiation was investigated using a co-culture system. The ability of basophils from patients with SLE with anti-dsDNA IgE to create cytokines that may be involved in B cell differentiation in response to dsDNA was examined using real-time PCR. Results: Anti-dsDNA IgE levels in the serum of patients with SLE correlated with disease activity. Healthy donor basophils produced IL-3, IL-4 and TGF-β1 after anti-IgE stimulation. Co-culture of B cells with anti-IgE-stimulated basophils increased plasmablasts which were cancelled by neutralizing IL-4. After encountering the antigen, basophils released IL-4 more quickly than follicular helper T cells. Basophils isolated from patients with anti-dsDNA IgE promoted IL-4 expression by adding dsDNA. Conclusions: These results suggest that basophils contribute to the pathogenesis of SLE by promoting B cell differentiation via dsDNA-specific IgE in patients similar to the process described in mouse models.

DOI： 10.1093/rheumatology/kead082

Web of Science

Scopus

PubMed

Language：Japanese  

Language：Japanese  

Language：Japanese  

Language：Japanese  

Language：Japanese  

Language：Japanese   Publisher：(株)日本臨床社  

Language：Japanese   Publisher：(有)科学評論社