Cowan F M, Klein D L, Armstrong G R, Pearson J W
Biomedicine. 1979 Nov;30(5):241-4.
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.
将金黄色葡萄球菌蛋白A注射到先前已接触过抗原（绵羊红细胞）的小鼠体内，能够增强或抑制原发性迟发型超敏反应（DH）。当给予大于最佳致敏剂量的抗原时，SPA可增强对SRBC的DH反应。在引发对SRBC的DH的最佳抗原剂量下，SPA抑制了DH。金黄色葡萄球菌蛋白A作用的一种推测机制是基于该蛋白作为Fc细胞受体发挥功能的能力，从而中和抗原-抗体免疫复合物对DH的影响。蛋白A与抗原-抗体免疫复合物的Fc部分结合有效地阻止了这些复合物随后与Fc细胞受体的结合，从而消除了它们作为细胞间免疫通讯辅助因子的参与。蛋白A既能增强又能抑制DH，这表明血清因子和/或细胞受体的相对浓度在原发性DH反应的调节中起作用。
