Endocrine Abstracts (2009) 20 P22

Role of chemokines MIP1[alpha] and MIP1[beta] in patients with Addison's disease isolated or associated to autoimmune thyroid disease

Annamaria De Bellis1, Elena Pane1, Marina Battaglia1, Giuseppe Ruocco1, Gilda Tirelli1, Giuseppe Bellastella1, Antonio Agostino Sinisi1, Costantini Susan2, Francesca Capone2, Annarita Aiello Talamanca2, Rosa Calemma3, Antonio Bizzarro1 & Antonio Bellastella1

1Department of Clinical and Experimental Medicine and Surgery, Chair of Endocrinology and Chair of Immunology and Allergology, ‘F. Magrassi, A. Lanzara’, Second University of Naples, Naples, Italy; 2Research Oncological Centre of Mercogliano, Mercogliano, Italy; 3UOSC of Immunology, IRCCS National Tumoral Institute of Naples, Naples, Italy.

High levels of macrophage inflammatory proteins (MIP1α and MIP1β), related to the recruitment of Th1 and Th2 cells, respectively, have been evidenced in some organ and non organ-specific autoimmune diseases. CXCL10/IP10 has been evidenced in patients with autoimmune thyroid disease (ATD) and in Addison’s disease (AD); MIP1α and MIP1β chemokines have not been so far evaluated in these diseases.

Aim: To evaluate plasmatic levels MIP1α, MIP1β and IP10 in patients with AD isolated or associated to ATD. MIP1α, MIP1β and IP-10 were evaluated in the plasma of 11 patients with AD associated to ATD (group 1), 8 patients (group 2) with isolated AD and 30 healthy controls (kit Bio-Plex Human Cytokine Assay). All patients were treated with an appropriate substitutive therapy, except 1 patient of group 1 and 2 of group 2 who had a new diagnosis of AD. The levels of MIP1α and MIP1β resulted significantly high (P<0.001) in both groups with respect to controls. No significant difference was observed between the two groups. Moreover, levels of MIP1β were significantly and positively related to the titre of adrenal autoantibodies and were inversely correlated to the duration of the disease.

The presence of high levels of MIP1α and MIP1β not only in cases of autoimmune isolated AD, but also in those ones associated to ATD seems to indicate a role of these chemokines in the autoimmune pathology of these glands mediated by the recruitment in loco of Th1 and Th2 cells. The reduction of MIP1β, inversely correlated to the duration of the disease, seems to indicate a predominant role of these chemokines in triggering an inflammatory process by a massive recruitment of Th2 cells. Instead, the persistent high levels of MIP1α during the disease seem to favour a chronic autoimmune process by constant recruitment of Th1 cells.