The autoimmune disorder systemic lupus erythematosus (SLE) involves upregulation of IgD, and studies have shown that anti-IgD antibodies can alleviate the autoimmune disorder rheumatoid arthritis in mouse models. Building on this finding, researchers in Hefei and Changshu, China, have shown that interrupting the interaction between IgD and its receptor FcδR can reduce cytokine levels and phosphorylation of JAK2 and STAT3, suppressing the activation and proliferation of CD4+ T cells in SLE.