Bruton’s tyrosine kinase (BTK), a member of the Tec family of nonreceptor tyrosine kinases, promotes B-cell growth, maturation, migration, and apoptosis. In addition, BTK signaling is involved in innate immune responses and regulates the production of proinflammatory cytokines. Cancer, autoimmunity, or inflammation may be a result of dysregulated BTK pathways. Studies have verified BTK as an essential target for agents against chronic lymphocytic leukemia (CLL).
BTK is primarily expressed in most hematopoietic cells such as B cells, mast cells, and macrophages, with the exception of T cells and terminally differentiated plasma cells. BTK is localized in bone marrow, spleen, and lymph node tissue. BTK is involved in the signaling pathway of low-affinity activating-Fcγ receptors for the immunoglobulin G (IgG)-containing immune complexes in monocytic cells. The Fcγ receptor signaling is present in mast cells and basophils that trigger the expression of pro-inflammatory cytokines, chemokines, and cell adhesion molecules.
