Surface polysaccharide antigens, expressed by strains of P. aeruginosa, are readily available for interaction with the host immune systems. These interactions could potentially result in development of protective immunity against P. aeruginosa infections. Classic strains of P. aeruginosa isolated from immunocompromised hosts and the environment generally express cell surface LPS antigens containing the serotype determinant. Antibody to these determinants has clearly been shown to be protective in both animals and humans. Immunization with a nontoxic, high molecular weight polysaccharide fraction, obtained from the culture supernate of P. aeruginosa, results in the induction of high titered, functional antibody against the type specific determinant. In addition, experimental protocols in animals have shown that a T cell-mediated immunity against type specific antigens can also provide protective immunity. Although the role of T cell-mediated immunity in protection against P. aeruginosa infections is unclear, it may be important in augmenting antibody-mediated protection. P. aeruginosa isolates from CF patients generally do not express type-specific antigens. They do, however, express a different cell surface polysaccharide, MEP. Antibody to this material is made by the colonized CF host, but it clearly is not associated with protective immunity. Animal antibody raised to this material is able to mediate opsonic killing of mucoid strains of P. aeruginosa. Therefore, the antibody response to MEP made by the CF patients may be non-opsonic, or if opsonic, may indicate that antibody to this antigen is not protective in CF patients. Antibody to MEP is able to interact with a low level of human complement for opsonic killing, suggesting that this antibody may be of use in the lung of the CF patient, where complement components may be either low or inactive.