Platelet aggregation and aggregation inhibition by different antiglobulins and antiglobulin complexes from sera of patients with rheumatoid arthritis.

Antiglobulin complexes were isolated from rheumatoid arthritis (RA) sera in order to investigate their ability to aggregate human platelets and to influence platelet aggregation induced by heat-aggregated IgG. Eleven of 38 seropositive RA sera showed a significant platelet aggregation (PA) titer as compared to 40 normal control sera. No correlation was observed between sheep T cell agglutination titers and PA titers of individual sera. Ten of 22 RA antiglobulin preparations containing IgG, IgM, and IgA antiglobulins and antiglobulin complexes also showed positive PA tests. Such preparations were able to inhibit PA brought about by heat-aggregated human IgG. When IgG and IgM antiglobulins were tested separately, only IgM antiglobulins showed this inhibitory effect, whereas IgG antiglobulins were inactive. Neither IgG nor IgM antiglobulins induced PA alone. Reassociated IgG antiglobulin complexes consisting of carefully prepared IgG and isolated IgG antiglobulins were able to induce PA. Platelet aggregation by RA sera was thus shown to be due to IgG antiglobulin complexes present in the sera. It can be concluded from these experiments that the composition of antiglobulin complexes in individual sera comprised of antiglobulins of different classes and IgG “antigen” is responsible for PA results in vitro. In pathophysiologic terms, the reaction of IgG antiglobulin complexes with thrombocytes in vivo may be an important step in the chain of events leading to generalized vascular damage and deposition of immune complexes in vessel walls which is thought to be responsible for the development of generalized vasculitis in RA.