PTPN22 function is regulated by reactive oxygen species, and redox regulation of PTPN22 impacts T-cell-dependent autoimmune inflammation.

Humans with mutations in the AIRE gene exhibit common autoantibodies targeting ovarian and intestinal antigens, including intestinal dysfunction-associated antibodies to enteroendocrine transcription factor RFX6.

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

Cell biology and animal model analysis in mice shows that molecules involved in glycolytic metabolism could potentially serve as therapeutic targets for the treatment of neurological diseases.

The three-dimensional architecture of the genome in distinct cell types predicts genes and regulatory elements involved in cell function and disease.

PDGFRα+ Sca-1+ bone marrow stromal/stem cells in whole bone marrow grafts can trigger the onset of autoimmune-related fibrosis in a mouse model of scleroderma.

Alteration of host gut microbiota by antibiotic exposure in early life remodeled host intestinal immune development and metabolism and enhanced the induction of type 1 diabetes in genetically predisposed animals.

Genetic variations that underlie common autoimmune disease genes are predominantly regulatory and modify the expression of multiple genes within the HLA gene complex and throughout the immune system.

Treatment with a JAK inhibitor normalizes multiple biomarkers of autoinflammation and provides therapeutic benefit for diverse immune skin conditions in individuals with Down syndrome.

Single-cell analysis revealed that autoantigen-reactive B cells changed the type of cytokines they produced from anti-inflammatory IL-10 and IL-35 to pro-inflammatory IL-6 and IL-23 as affinity to autoantigen increased.