Chronic Spontaneous Urticaria and Bruton Tyrosine Kinase: A Multispecialty Expert Discussion

Panelists discuss how chronic spontaneous urticaria involves autoantibody-mediated mast cell activation and degranulation, with BTK serving as a critical signaling molecule in both mast cells and B cells that produce pathogenic autoantibodies.

Panelists discuss how chronic spontaneous urticaria develops through 2 distinct pathways: autoallergic CSU involving IgE-mediated mast cell activation (type I hypersensitivity) and autoimmune CSU where IgG autoantibodies target FcεRI receptors or IgE itself (type IIb hypersensitivity), both ultimately leading to mast cell degranulation and wheal formation.

Panelists discuss how chronic spontaneous urticaria (CSU) treatment targets multiple pathways through antihistamines, anti-IgE therapy, and BTK inhibitors, with BTK emerging as a key target.

Panelists discuss how Bruton tyrosine kinase (BTK) inhibition could effectively treat both autoallergic and autoimmune chronic spontaneous urticaria (CSU).

Panelists discuss how Bruton tyrosine kinase (BTK) inhibitors offer a novel upstream approach, in contrast to current treatments that work downstream by either blocking released mediators (antihistamines), neutralizing circulating IgE (omalizumab), or broadly suppressing immune responses (immunosuppressants).