Bruton’s tyrosine kinase (BTK) mediates B cell signaling and is also present in innate immune cells but not T cells. BTK propagates B cell receptor (BCR) responses to antigen-engagement as well as to stimulation via CD40, toll-like receptors (TLRs), Fc receptors (FCRs) and chemokine receptors. Importantly, BTK can modulate signaling, acting as a “rheostat” rather than an “on-off” switch; thus, overexpression leads to autoimmunity while decreased levels improve autoimmune disease outcomes. Autoreactive B cells depend upon BTK for survival to a greater degree than normal B cells, reflected as loss of autoantibodies with maintenance of total antibody levels when BTK is absent. This review describes contributions of BTK to immune tolerance, including studies testing BTK-inhibitors for treatment of autoimmune diseases.

Original languageEnglish
Pages (from-to)763-773
Number of pages11
JournalExpert Review of Clinical Immunology
Issue number7
StatePublished - Jul 2 2016


  • B lymphocyte signaling
  • BTK inhibitors
  • Bruton’s tyrosine kinase
  • autoimmune inflammatory arthritis
  • autoimmunity
  • systemic lupus erythematosus
  • type 1 diabetes


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