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Normal rabbit lenses exposed in vitro to heterologous antilens and antiuveoretina antibodies lose control of the intracellular 86Rb and this effect is followed by a late leakage of lenticular proteins; both phenomena take place only in the presence of complement. This antibody-induced complement-dependent membrane damage might be involved in the pathogenesis of complicated cataracts in uveitis and in the self-maintenance of recurrent uveal inflammations.
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