Using mice expressing a Bcl-2 mutant protein to suppress multiple central tolerance pathways, it is shown that central tolerance is crucial for preventing autoimmunity.

Galectin-9-deficient mice develop spontaneous autoimmunity, driven by a decreased threshold of B cell activation and enhanced auto-antigen delivery to the spleen by increased B1a-derived autoantibodies.

The development of Natural Killer T Cells is controlled by Histone Deacetylase 7, a function that combined with its known role in thymic negative selection provides a potential mechanism explaining its association with tissue-specific autoimmunity in humans.

By using immune cells called dendritic cells to deliver drugs, it is possible to target and kill specific members of another class of immune cell, known as T cells, and to prevent these cells from attacking the body's own tissues in cases of autoimmune disease.

A high-throughput extension of PhIP-seq reveals novel antigen specificities leading to new insights across multiple human autoimmune and inflammatory diseases, enables application of machine learning approaches to PhIP-seq datasets, and highlights the importance of controlled PhIP-seq cohorts.

Lymphocyte migration and autoimmunity induction rely on Formin-like 1-mediated actin network remodeling to push the lymphocyte nucleus through restrictive endothelial barriers.

Deficiency of capicua, a transcription factor that suppresses autoimmunity, impairs positive and negative selection processes by attenuating TCR signaling in CD4⁺CD8⁺ double-positive thymocytes.

Regulatory T cell suppress cytotoxic T cells in autoimmunity and cancer by taking up IL-2.

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.

Engineered T cell receptors enable targeted immunotherapy with a reduced risk of harmful autoimmunity.