A new study by Andrea Moy, Mandakolathur Murali and Rosalynn Nazarian, published in the Journal ofCutaneous Pathology, indicates that in the chronic urticaria skin lesions the immune response is characterized by a Th2/Th17 shift.
Chronic urticaria (hives) is a condition where an itchy rash persists on and off for six weeks or more.
The majority cases of chronic urticaria have unknown (idiopathic) causes, but more than 50% of the chronic idiopathic urticaria cases are thought to be driven by autoimmune mechanism(s). Furthermore, it appears that chronic urticaria is associated with other autoimmune diseases, such as thyroid disease, rheumatoid arthritis, systemic lupus erythematosus and Sjögren’s syndrome.
In the Journal ofCutaneous Pathology study, Moy et al., from the Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA report that Th17 and Th2 cells are significantly more frequent in chronic urticaria lesions, and their lymphocytic infiltrate, as compared with normal skin. In apparent contrast, there was no significant difference in mast cells, Th1 or Th22 cells.
Of note, in samples from patients with and without markers of autoimmunity, and/or thyroid disease, there was no significant difference in the number of mast cells or percentage of Th1, Th2 and or Th2.
Interestingly, samples from patients with both chronic urticaria and autoimmune diseases were characterized by a significant reduction in Th22 cells numbers, and an increased density of mast cells.
In conclusion, the study indicates that in chronic urticaria the local skin immunity is skewed towards a Th2/Th17 shift, without the presence of mast cell prevalence in the lymphocytic infiltrate, and perhaps, no evidence that an additional autoimmune disease contribute to this immune phenotype.