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Platelet phagocytosis in the spleen of patients with idiopathic thrombocytopenic purpura (ITP)
Author(s) -
LUK S.C.,
MUSCLOW E.,
SIMON G.T.
Publication year - 1980
Publication title -
histopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.626
H-Index - 124
eISSN - 1365-2559
pISSN - 0309-0167
DOI - 10.1111/j.1365-2559.1980.tb02906.x
Subject(s) - phagocytosis , platelet , red pulp , thrombocytopenic purpura , spleen , marginal zone , antigen , white pulp , antibody , immunology , chemistry , degranulation , pseudopodia , biology , biochemistry , receptor , cell , b cell
The ultrastructure of spleen from four patients with idiopathic thrombocytopenic purpura (ITP) is studied. Platelets, with no evidence of degranulation and aggregation, leave the circulation by passing through gaps in the sinus wall in the marginal zones and the red pulp. They are then trapped by pseudopods of macrophages and are phagocytosed as whole elements. The endothelial cells lining the sinuses do not phagocytose platelets or other circulating blood cells. The degradation of these platelets in the phagolysosomes of macrophages is incomplete and results in the formation of myelinic‐like figures which accumulate in large numbers in these cells. This incomplete platelet breakdown may be due to a deficiency of specific lysosomal enzymes. Erythroleucophagocytosis in ITP is normal. The results are consistent with the concept that ‘self’ constituents are normally and readily destroyed by autolytic enzymes. In the case of enzyme deficiency or the presence of ‘foreign’ antigens, including altered ‘self’ antigens, these enzymes become ineffective for rapid and complete degradation of the substrate. Through macrophage‐lymphocyte interaction, antibody‐forming cells are activated against these residual substances. These antibodies, in turn, facilitate the phagocytosis of the specific ‘antigens’ by macrophages. The massive platelet phagocytosis and the presence of large numbers of germinal centres in the white pulp and plasma cells in the marginal zone and red pulp suggest that the spleen is the major site of platelet destruction, as well as the site of antiplatelet antibody synthesis.