NOTICE: Labnodes now supports vumc.org email addresses. If your email changed, please update your profile today.

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

Connections (2)

This publication is referenced by other Labnodes entities:

Links