Autoimmune disease affects ~5% of individuals globally, and the prevalence is increasing. The cause of diseases such as Systemic Lupus Erthematosus (SLE) and Rheumatoid Arthritis (RA) remains largely unknown and commonly used therapeutic agents present with considerable side effects.

Detection of autoantibodies is a common feature of many autoimmune diseases, including SLE and RA. Due to inherent signaling defects B cells produce autoantibodies and directly contribute to the pathogenesis of disease. The Germinal Centre (GC) reaction is therefore a pivotal step in this process, allowing B cells to undergo affinity maturation and differentiation into long-lived plasma cells. While CD4+ Follicular helper T cells (Tfh) migrate into B cell follicles and engage GC B cells to generate antibody responses. This critical collaboration dictates the production of high affinity antibodies, or autoantibodies when the signaling circuitry is altered in B cells or Tfh cells.

Understanding the molecular pathways that contribute to autoimmune disease remains a high priority, particularly during atypical T and B cell interactions. Aside from finding novel drug targets, the identification of biomarkers can confer disease diagnosis and provide valuable information about the treatment regimens and prognosis.

The aim of this Research Topic is to highlight and discuss our current understanding of key signaling pathways that become deregulated in B or T lymphoid cells and contribute to the pathogenesis of autoimmune disease. Emphasis is placed on understanding the roles of prominent Kinases or Transcriptional Regulators that contribute to the control of cell survival, proliferation and differentiation, or regulate cell extrinsic processes by deregulating the production of key cytokines and chemokines.

Keywords: Kinases, Cell Signalling, Autoimmunity, Transcription Factors

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