Abstract
In recent years, the demonstration of circulating functional autoantibodies against the high affinity IgE receptor or against IgE themselves in about one-third of patients with chronic idiopathic urticaria has suggested that an autoimmune mechanism might be involved in the pathogenesis of the disease [the so-called chronic autoimmune urticaria (CAIU)]. In this study we compare findings from serum-induced and spontaneous wheals with regard to immunohistochemical markers of disease activity and discuss whether autologous serum skin test (ASST) may be regarded as an in vivo experimental model of the physiological stimulus causing urticaria skin condition, or if it does not reproduce the whole of the mechanisms operating in the development of spontaneous wheals. By means of immunohistochemical technique, we analyzed specimens from just-developed spontaneous wheals and from serum-evoked wheals of six CAIU patients, to glean information on cellular infiltrate and related cytokines, chemokines, chemokine receptors and adhesion molecules. According to the results of our study, spontaneous urticaria lesions seem to be sustained by a characteristic inflammation pattern where neutrophils, adhesion molecules, IL-8 and chemokine receptors play a main role in flogosis triggering and, consequently, disease development. On the contrary, ASST-induced wheals seem to imply different activities mainly represented by basophil granulocytes and related molecules, i.e. IL-4. Although it represents an efficacious diagnostic instrument to screen CAIU patients, ASST is not an exhaustive model of the many immunopathogenic pathways operating in the development of urticaria lesions, especially with regard to systemic activation networks.