Anti-idiotype immunomodulation of experimental anti-phospholipid syndrome via effect on Th1/Th2 expression

Mice with experimental anti-phospholipid syndrome (APS), induced by active immunization with a human anti-cardiolipin MoAb (H-3), were treated with mo use anti-idiotypic MoAb (anti-H3, named S2.9) and with an irrelevant anti-i diotype. The immunized mice produced high titres of mouse anticardiolipin a ntibodies along with clinical manifestations of experimental APS: prolonged activated partial thromboplastin time (aPTT), thrombocytopenia and high ra te of fetal loss. Treatment with the specific anti-Id (S2.9) as a whole mol ecule or F(ab)(2) fraction, resulted in a decrease in serum levels of the a nti-cardiolipin antibodies, rise in platelet count, shortened aPTT and redu ced rate of fetal loss. The anti-Id effect was associated with a rise in th e number of IL-2 and interferon-gamma (IFN-gamma)-secreting cells (Th1) and reduction in IL-4- and IL-6-secreting cells (Th2). The beneficial effect o f the anti-Id treatment in mice with experimental APS induced by active imm unization with an idiotype further supports the idiotypic aetiology of expe rimental APS and points to the role of Th1 cytokines in suppression of its manifestations.