The interactions between blood and insoluble polysaccharidic surfaces result in activation of the immune system of complement. When substituted with carboxymethyl groups, Sephadex loses its capacity to activate complement, whereas Sephadex sulphate has been described as an activator. In order to elucidate the molecular mechanisms of complement activation and inhibition, a simpler polymer model has been choosen: it consists of an insoluble polystyrene backbone on which either isolated hydroxymethyl or sulphonate groups or both are present. The surfaces bearing the isolated groups consume complement but the mechanisms involved are quite different. In contrast, a surface bearing equal proportions of both types of groups is a non-activator. Such model surfaces can be very useful for designing artificial surfaces able to control in situ complement activation.