According to the findings of a recent study, basophils in chronic urticaria demonstrate an increased ability to migrate to the skin, which is amplified by immunoglobulin E (IgE)-mediated stimulation. The objective of the study was to characterize the ability of basophils in chronic urticaria to migrate to specific skin locations, evaluate the receptor profile associated with these basophils, and examine the impact of Omalizumab treatment on these factors.

Flow cytometry was utilized to examine unstimulated and activated basophils from 11 chronic urticaria patients undergoing Omalizumab treatment and 10 healthy individuals. The study focused on evaluating the expression of various receptors in these basophils upon stimulation with anti-IgE, formyl-methionyl-leucyl-phenylalanine (fMLP), C5a, and Substance P. In chronic urticaria patients, unstimulated basophils displayed elevated levels of skin-associated receptor CCR8 and scavenger receptor CCX-CKR, along with decreased expression of the lung-associated receptor CCR3, in comparison to healthy subjects.

IgE-mediated activation further heightened percentage of CCX-CKR and CCR8 receptors in chronic urticaria volunteers contrasted to healthy group. Additionally, it led to increased expression of lung-associated chemokine receptor XCR1 in both chronic urticaria patients and healthy subjects. Basophils in chronic urticaria displayed an increased expression of the coagulation cascade receptor (CD87) and the fMLP receptor (FPR1), indicating an augmented response. Conversely, there was a tendency towards reduced expression of the immunotolerance receptor (CD109) and the itch receptor (IL-31RA) on chronic urticaria basophils.

Stimulation with C5a and fMLP resulted in enhanced expression of CCX-CKR, CCR8, CCR4, and CD87, while reducing the expression of CCR3 and CCR2. However, no discernable differences were witnessed between chronic urticaria and healthy groups in these changes. Hence, basophils in chronic urticaria demonstrate an increased potential to migrate to the skin, which is further amplified by IgE-mediated stimulation.