The sialylation of RANK⁺TLR2⁺ monocytes contributes to osteoclastogenesis and bone destruction in rheumatoid arthritis.

Cellular immunological and biochemical analyses reveal how decoy IL-1RII is induced by human CD4⁺ T cells upon TCR-stimulation and regulates the Th17-Treg balance by modulating IL-1β responsiveness in IL-1RI⁺ cells.

Phosphorylation-mediated inactivation of pro-apoptotic BCL-2 family protein BAD confers the apoptosis resistance on synovial sublining macrophages, thereby contributing to the development of rheumatoid arthritis.

MiR 204/211 antagonize synovial inflammation and hyperproliferation by regulation of its downstream target gene Ssrp1, and decelerated RA progression.

SARS-CoV-2 experienced ocrelizumab-treated MS patients benefit from SARS-CoV-2 mRNA vaccination by inducing broadprotective CD8+ T-cells, whereas methotrexate-treated RA patients induce delayed but strong antibody responses, which support vaccine strategies for these patient groups.

Microbial populations are continuous along the gastrointestinal tract, with increased transmission in colorectal cancer and rheumatoid arthritis patients.

A new role is identified for GLI1 in modulating the inflammatory response of macrophages and the overaction of osteoclasts in collagen-induced arthritis by collaboratively regulating DNMT1 and DNMT3a.

The sequencing of microbial genomes reveals that the presence of a particular microbial species in the gut may increase the risk of the autoimmune disease rheumatoid arthritis.

A subtype of myeloid monocyte mediates the transition from autoimmunity to joint destruction in rheumatoid arthritis.