Chronic urticaria serum-induced CD63 expression assay performed on DA whole blood by means of our tricolour FCM method could be the most useful tool for identification of a subset of patients with autoimmune CU and may become a promising tool also for monitoring treatment efficacy.
A total of 97 patients with atopic dermatitis (AD), 123 patients with chronic urticaria (CU), 286 children with asthma, and control groups were screened for polymorphisms in the promoter region located upstream of FCER1A exon 1 by the polymerase chain reaction-ligation detection reaction method.
As the role of CTLA-4 polymorphism in autoimmune thyroid diseases is well proven we speculated on the possible role of this polymorphism in the background of chronic urticaria.
Association of insertion/deletion polymorphism of the angiotensin-converting enzyme gene with angio-oedema accompanying chronic urticaria but not chronic urticaria without angio-oedema or the autologous serum skin test response.
Functional autoantibodies against the alpha-chain of the high-affinity IgE receptor (FcepsilonRIalpha) identify a subset of patients with chronic urticaria (CU) due to autoreactivity, as assessed by an in vivo positive response to autologous serum skin test (ASST).
In addition, both chronic urticaria and C1-INH deficiency can be associated with other autoimmune diseases, although the importance of these associations remains to be determined.
Other promising drugs that are currently under development for CU are a chemoattractant receptor-homologous molecule expressed on T<sub>H</sub>2 cell antagonist, a monoclonal antibody to Siglec-8 (AK002), Bruton tyrosine kinase inhibitors (fenebrutinib and Lou064), a spleen tyrosine kinase inhibitor, and dupilumab.
Other promising drugs that are currently under development for CU are a chemoattractant receptor-homologous molecule expressed on T<sub>H</sub>2 cell antagonist, a monoclonal antibody to Siglec-8 (AK002), Bruton tyrosine kinase inhibitors (fenebrutinib and Lou064), a spleen tyrosine kinase inhibitor, and dupilumab.
Other promising drugs that are currently under development for CU are a chemoattractant receptor-homologous molecule expressed on T<sub>H</sub>2 cell antagonist, a monoclonal antibody to Siglec-8 (AK002), Bruton tyrosine kinase inhibitors (fenebrutinib and Lou064), a spleen tyrosine kinase inhibitor, and dupilumab.