Lipopolysaccharide-responsive (LPS(r)) and LPS-defective (LPS(d)) strains of C3H mice differ greatly in the capacity of bacterial monophosphoryl lipid A (MPL) to inactivate suppressor T cell (Ts) function generated after exposure to Type III pneumococcal polysaccharide (SSS-III). This suggests that the activated Ts of such mice differ with respect to (a) a cell surface receptor required for the binding and subsequent internalization of MPL and/or (b) the presence of a biochemical pathway that is extremely sensitive to inactivation by MPL. The predominant isotype of antibody against Pseudomonas aeruginosa LPS in several strains of inbred mice is IgG3. Treatment with Gamma-interferon resulted in an increase in IgG2a antibody, regardless of major histocompatibility complex (MHC) haplotype. Thus the isotypic pattern produced in mice immunized with this antigen is not MHC restricted and is influenced greatly by lymphokines.
