[2] The experiment was undertaken in 1950 by William J. Harrington and James W. Hollingsworth, who postulated that in patients with idiopathic thrombocytopenic purpura (ITP), it was a blood factor that caused the destruction of platelets.
[2] Bone marrow biopsy from Harrington's sternum demonstrated normal megakaryocytes, the cells necessary for platelet production.
[2] Schwartz notes that the Harrington–Hollingsworth experiment was a turning point in the understanding of ITP's pathophysiology: The Harrington–Hollingsworth experiment changed the meaning of the "I" in ITP from idiopathic to immune, but "immune" in this case means "autoimmune," because the antibodies bind to and cause the destruction of the patient's own platelets.
[2] This suggested that low platelet counts (thrombocytopenia) in patients with ITP was caused by a circulating factor found in the blood.
[3][4] Many physician-scientists believe the findings had a major influence on the field of autoimmunity, which was not universally accepted at the time as a mechanism of human disease.