Augmentation and inhibition of delayed hypersensitivity by Staphylococcus aureus protein A.

The injection of Staphylococcus-aureus protein A into mice, previously exposed to an antigen (sheep red blood cells), is capable of augmenting or inhibiting a primary delayed hypersensitivity (DH) response. SPA enhances DH response to SRBC when given with a greater than optimal sensitizing dose of the antigen. At antigen doses optimal for eliciting DH to SRBC, SPA inhibited DH. A proposed mechanism for the action of Staphylococcus-aureus protein A is based upon the ability of the protein to function as a Fc cellular receptor, thus neutralizing the effect of antigen-antibody immune complexes on DH. The binding of protein A to the Fc portion of antigen-antibody immune complexes effectively prevents subsequent binding of these complexes to Fc cellular receptors, thus eliminating their participation as co-factors in inter-cellular immunological communication. The ability of protein A to both augment and inhibit DH suggests a role for relative concentrations of serum factors and/or cellular receptors in the regulation of a primary DH response.