Antibodies reactive with surface membranes of cellular elements in the blood

Autoreactive antibodies or immune complexes may accelerate clearance of mature erythrocytes, leukocytes, and platelets from the circulation in patients with rheumatologic and immunologic disorders. The most compelling evidence for immune injury to hematopoietic cells exists in patients with systemic lupus erythematosus and patients with Felty's syndrome and its variants. These disorders may also cause tissue inflammation, which in turn commonly results in underproduction of erythrocytes and development of thrombocytosis. However, recent evidence indicates that underproduction of hematopoietic cells may also result from immune injury to cellular elements in the bone marrow. In many laboratories, sensitive techniques are now clinically available for the detection of cell-associated immunoglobulin and complement. These assays have helped confirm the role of antibody in the pathogenesis of autoimmune hemolytic anemia and idiopathic thrombocytopenic purpura. However, recent data indicate that there is probably a continuum between the amount of immunoglobulin and complement found on normal cells and that found in a variety of disease states. In several of these disorders, additional evidence will be required to establish that the increase in cell-bound immunoglobulin leads to a decrease in the life-span of the cell. In order to provide significant help to the clinician managing an individual patient, these serologic tests must be capable of identifying the portion of the cell-associated protein actually involved in the destructive process. The availability of monoclonal reagents capable of identifying restricted regions on cell-bound immunoglobulin may help identify molecules bound specifically as antibody and may help identify the antigens involved in autoimmune disorders.