Imbalance in Th1 and Th2 subsets and their derived cytokines seems to be involved in the immune abnormalities underlying UC and CD. CD30 is a member of the tumour necrosis factor/nerve growth receptor superfamily expressed on T cells producing Th2 cytokines and released as a soluble form. In this study high levels of soluble CD30 were found in sera of UC patients independently of disease activity. Furthermore, increased titres of soluble CD30 molecule were shown, in the same patients, by mitogen-stimulated cultures of peripheral blood mononuclear cells. Our data seem to indicate that an activation of Th2 immune response is involved in the pathogenesis of UC, but not of CD. Furthermore, this finding indicates that serum soluble CD30 measurement may be helpful for differentiating these two forms of inflammatory bowel disease.

In a previous study, we showed an imbalance in the cytotoxic phenotype of circulating PBMC of IBD patients, possibly related to an alteration in the cytotoxic activity, which might play a role in the immunopathogenesis of IBD. γ/δ T cells, which are increased in the PBMC of IBD patients, represent a minor population of peripheral lymphocytes displaying cytolytic potential and showing both MHC and non-MHC cytotoxicity. This study was performed in order to verify their role in the cytotoxic activity of PBMC from IBD patients and correlate this activity to UC and CD, respectively. We observed a decreased NK cytotoxicity of PBMC in both UC and CD patients and this findings was unrelated to γ/δ T lymphocytes. In fact, both total and γ/δ-depleted PBMC of IBD patients, showed comparable lytic activity. On the contrary, the ADCC lytic activity was within normal range in our patients, ad was not modified by removal of γ/δ cells. The increase of Vδ1+ T cells, previously observed in our patients, seems to be unrelated to this functional impairment, because of a low cytotoxic activity displayed by this subset. Alternatively, the expanded Vδ1+ T cells could be involved in the pathogenesis of the autoimmune phenomena observed in IBD, by a mechanism different from cytotoxicity, such as autoantibodies production and/or loss of tolerance.

Vasculitides are a set of serious diseases of unknown aetiology with various immunopathogenetic mechanisms, characterized by inflammation and necrosis of the vessel wall with consequent lumen obliteration. They may be primitive or associated with other diseases, have heterogeneous clinical manifestations and different degrees of severity which may be related to the localization of the interested vessels. Although in the last years many classifications have been proposed, a standardized nomenclature of vasculitides is unquestionably still needed to facilitate the diagnosis and management of patients with the disease. Steroids and immunosuppressant are the conventional therapy, whereas other therapeutic strategies are reserved for the refractory vasculitides to conventional therapies or for intolerant recipients to cytotoxic drugs. New approaches are represented by monoclonal antibodies and drugs which could be effective in the treatment of the trigger factors which activate the immunopathological mechanisms. Current data suggest that, rather than pursuing the idea of a single therapy for vasculitides, an oncological model of combined therapy, to induce both the disease control and maintenance of remission, might be adopted. An improvement of our knowledges on the mechanisms underlying the different entities associated to standardized criteria of activity and remission of disease will lead to an improvement of our therapeutic strategies.