The role of Bruton's tyrosine kinase in autoimmunity and implications for therapy.

Crofford LJ, Nyhoff LE, Sheehan JH, Kendall PL
Expert Rev Clin Immunol. 2016 12 (7): 763-73

PMID: 26864273 · PMCID: PMC5070917 · DOI:10.1586/1744666X.2016.1152888

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.

MeSH Terms (12)

Animals Anti-Inflammatory Agents Autoantibodies Autoimmune Diseases Autoimmunity B-Lymphocytes Humans Immune Tolerance Lymphocyte Activation Protein-Tyrosine Kinases Receptors, Antigen, B-Cell Signal Transduction

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