1. There are two possible ways in which platelets may be involved in immune reactions: a) as target cells for antiplatelet antibodies, and b) as receptor cells for circulating antigen-antibody complexes. Since most of the clinical tests used to detect "antiplatelet antibodies" are incapable of discriminating between the two mechanisms, thrombocytopenia in many autoimmune diseases with "antiplatelet antibodies" may well be caused by immune complexes. 2. Immune reactions involving platelets do not always lead to thrombocytopenia. A moderate acceleration of platelet destruction can easily be compensated by increased production: this situation corresponds to a "compensated thrombocytolytic state". Evidence is also presented for immunologically induced functional platelet defects of "immunologic thrombocytopathy.