Serum Antibody & Th2 Cytokine Profiles in Patients with Cystic Echinococcosis (Report)
Human cystic echinococcosis (CE), caused by Echinococcus granulosus, is one of the most important and widespread parasitic zoonoses (1). In general human CE is diagnosed and characterized in the late symptomatic stages when significant pathology has already occurred (2). Many (60-80%) confirmed CE patients only are seropositive for antibodies (3), which may be due to the antibodies forming immune complexes in some patients (4). Several studies have shown an elevated IgG subclass (IgG1 and IgG4) antibody response in advanced human CE (5). While parasite-specific antibodies appear not to exhibit a direct restricting role on the growth of metacestodes in humans, the immunological effector function may be attributed primarily to T cells (6). Both humoral and T-cell mediated responses, constituted of T helper cell-1 (Th1) and T helper cell-2 (Th2) type reactions, seem to play an important role against infections and are considered to be regulated by cytokines (7). Th1 cells produce interferon-[gamma] (IFN[gamma]), interleukin, (IL-2), tumour necrosis factor-P (TNFP), and are responsible for both humoral and cell-mediated immune responses (8). Th2 cells produce IL-4, IL-5, IL-6, IL-9, IL-10 and IL-13 cytokines, which facilitate the production of IgE, IgG1-IgG4 isotype switching and IgA synthesis (8). Th2 type responses are predominant in patients with chronic extracellular parasite infections (9). IgG1 and IgG4 appear to be the most active antibody subclasses in both human cystic and alveolar echinococcosis (5). Fauser and Kern (10) have demonstrated that re-stimulation with crude E. granulosus antigen induced or enhanced Th2 cytokine mRNA expression (especially IL-5 and IL-10) by peripheral blood mononuclear cells from patients with CE. Another study showed a decrease in IL-1 and TNF cytokine levels in CE patients compared to controls (11).