A study led by Prof Alexander Weber from University of Tübingen now points to a new way to inhibit inflammation. A discovery that would have implications in the treatment of many diseases such as gout, Alzheimer's, atherosclerosis, heart attack or stroke. The paper, titled “Human NLRP3 inflammasome activity is regulated by and potentially targetable via BTK,” is published in Journal of Allergy and Clinical Immunology. Inflammation is the body's attempt to remove harmful stimuli, including damaged cells, pathogens and irritants, and to initiate healing of tissue. It is a protective response involving host cells, blood vessels and proteins. However, inflammation is also a potentially harmful process. For example, in atherosclerosis, inflammation can deteriorate the condition. The activation of inflammatory processes is driven by the inflammasome, a multiprotein oligomer that is expressed primarily by myeloid cells. The inflammasome is known to promote the maturation of inflammatory cytokines, but how it works is not fully understood. Weber’s team discover that an enzyme called Bruton's tyrosine kinase (BTK) serves as a regulator of inflammasome activation. It is possible to inhibit inflammation at early stage by targeting BTK. BTK is essential for B cell maturation and mast cell activation. Mutations in BTK have been suggested to cause the rare genetic immunodeficiency X-linked agammaglobulinemia (XLA). People with XLA have very few B cells, specialized white cells responsible for making antibodies. Due to a lack of antibodies, they are more susceptible to infection. For the present study, the researchers found that BTK is a component of the inflammosome and people carrying a BTK mutation have defective inflammasomes. Inhibition of BTK by either pharmacological or genetic methods resulted in reduced inflammation. These data indicate that BTK could be a potent target for diseases associated with inflammation. Cusabio provides BTK, and mouse polyclonal antibody.
