Why human pemphigoid autoantibodies do not trigger disease by the passive transfer into mice?
25.01.2012
Sesarman A, Oswald E, Chiriac MT, Csorba K, Vuta V, Feldrihan V, Baican A, Bruckner-Tuderman L, Sitaru C.
?Immunol Lett. 2012;143(1):92-100
The autoimmune nature of several diseases has been demonstrated by reproducing human disease features in animals by the transfer of patient autoantibodies. However, the lack of pathogenicity of patients' autoantibodies in mice, has been assigned to a limited cross-reactivity of the autoantibodies with the murine tissue. Bullous pemphigoid (BP) is an inflammatory subepidermal autoimmune disease, in which blistering is caused by autoantibodies activating complement and granulocytes. In the present work, we investigated the interaction of patients autoantibodies with murine antigen, complement system and murine granulocytes. We have demonstrated, that although pemphigoid autoantibodies bound to murine skin in vitro and in vivo, they showed a lower capacity of activating murine complement and murine granulocytes when compared with the human innate immunity factors. Our results should greatly facilitate the design of more effective therapies for this and related autoimmune diseases.
