**Background of BTK Antibodies**
Bruton’s tyrosine kinase (BTK), a non-receptor kinase belonging to the Tec family, plays a crucial role in B cell development and activation. It is integral to B cell receptor (BCR) signaling, mediating downstream pathways that regulate proliferation, survival, and differentiation. Mutations in the *BTK* gene cause X-linked agammaglobulinemia (XLA), a primary immunodeficiency marked by absent mature B cells and antibodies, underscoring BTK’s essential function in adaptive immunity.
Structurally, BTK contains a pleckstrin homology (PH) domain for membrane localization, tandem SH3-SH2 domains for protein interactions, and a catalytic kinase domain. Dysregulated BTK activity is implicated in B cell malignancies (e.g., chronic lymphocytic leukemia, mantle cell lymphoma) and autoimmune disorders, making it a therapeutic target. Small-molecule BTK inhibitors (e.g., ibrutinib) are widely used clinically, but BTK-specific antibodies have emerged as valuable tools for research and potential therapeutics.
BTK antibodies are employed to detect BTK expression, study its activation state (e.g., phosphorylation status), or inhibit its function in experimental models. Therapeutic monoclonal antibodies targeting BTK or its signaling partners are under exploration to overcome resistance to small-molecule inhibitors or modulate immune responses. Their high specificity offers promise for precision therapy, though clinical applications remain investigational. Overall, BTK antibodies bridge mechanistic insights into B cell biology and the development of targeted immunotherapies.