First AD

Second AD

The Pathogenesis of CSU

Video content above is prompted by the following:

What have we learned about the possible mechanisms involved with CSU pathogenesis?

Can you describe autoimmune responses and the role of Burton’s tyrosine kinase (or BTK) as a mediator in mast cell degranulation and histamine release?

Evolving Perspectives and Treatment Strategies in Chronic Spontaneous Urticaria 

HCPLive® Peer Exchange panel discussions feature authoritative insights, opinions, and perspectives on important issues facing today's care professionals.

Peer Exchange

Chronic spontaneous urticaria (CSU) pathogenesis involves complex mechanisms, including autoimmune responses and mast cell activation. Autoimmune responses in CSU are characterized by the presence of autoantibodies targeting IgE or the high-affinity IgE receptor (FcεRI) on mast cells and basophils, leading to their activation and degranulation. Burton’s tyrosine kinase (BTK) plays a crucial role as a mediator in this process, facilitating mast cell degranulation and subsequent histamine release. Understanding these mechanisms is essential for developing targeted therapies to manage CSU effectively.

Panelists discuss how recent insights into chronic spontaneous urticaria (CSU) pathogenesis reveal potential autoimmune responses and highlight the role of Bruton  tyrosine kinase (BTK) as a key mediator in mast cell degranulation and histamine release.

Bringing CSU Back Under The House of Dermatology

Understanding the Chronicity of CSU