Acquired pelicle appears to contain primarily IgA and other proteins of salivary origin. With the increased time necessary for plaque formation, gingival crevicular fluid contributes proteins to the growing plaque accumulation. However, secretory IgA is still the major intact immunoglobulin in plaque samples since appreciable portions of the molecules bearing IgG determinants appear to be degraded to small fragments. Nevertheless, the amount of IgA present in plaque, which could be considered antibody, is too little to account for most of the plaque interactions. Since secretory IgA appears to be resistant to proteolytic degradation by a mixture of plaque enzymes, and IgA fragments are not prominent in plaque extracts, degradation of secretory IgA probably cannot explain the relatively low IgA levels in plaque. It has been shown that salivary IgA antibody can interfere with enzymes responsible for the plaque-forming potential of certain organisms. All the preceding evidence is consistent with our current contention that secretory IgA functions as blocking antibody to interfere with the formation of dental plaque. This could occur by direct inhibition of bacterial polymer formation or by direct or indirect inhibition of bacterial interaction with salivary constituents by secretory IgA. Less than 1% of the plaque interactions can probably be attributed to secretory IgA antibody. IgG may contribute even less since it is degraded.