Systemic lupus erythematosus articles from across Nature Portfolio

A single-agent fusion of human IL-2 and antiIL-2 antibody is discovered and engineered to selectively expand regulatory T cells and to treat autoimmune diseases.

Tph1 subset expresses IL21 to show B cell helper function, while Tph2 subset expresses high levels of cytotoxicity-related molecules and low IL21. Tph1 and Tph2 subsets exert distinct immunological functions in the clinical manifestations in SLE.

Systemic lupus erythematosus is associated with neurological impairment. Here the authors show that exposure of hippocampal neurons to lupus autoantibodies in mice initiates a neuroinflammatory state sustained by continuous HMGB1:RAGE signaling that can be reversed with an ACE inhibitor.

This Review discusses the interplay of the gut microbiome and the immune system in the context of systemic lupus erythematosus. Dysbiosis and gut-barrier dysfunction are implicated in promoting disease and are potential therapeutic targets.

Ribonucleoprotein complexes containing Xist, a long non-coding RNA involved in X chromosome inactivation, are immunogenic and promote autoimmune responses.

Age-related B cells (ABCs) have pathogenic roles in autoimmune diseases. Research has now identified ZEB2 as the transcription factor that mediates differentiation into ABCs.

Newly published European guidelines for the management of systemic lupus erythematosus (SLE) and lupus nephritis, specifically recommending early and aggressive use of new medications, signal that the old paradigm of SLE management is shifting. Although it presents challenges, this shift is welcome — and is likely to have far-reaching implications.

Variants in the HLA region on chromosome 6 are strongly associated with many immune-related diseases. A method to construct personalized HLA genomes from single-cell RNA sequencing data, coupled with single-cell HLA expression quantitative trait loci modeling, identifies how genetic variants influence HLA gene expression across cell states.

Chromatin accessibility of an enhancer that regulates the expression of a disease-associated microRNA is affected in monocytes from patients with systemic lupus erythematosus, highlighting this enhancer as a potential therapeutic target.