Monocyte-platelet interaction in immune and nonimmune thrombocytopenia

M. N. Saleh, D. L. Moore, J. Y. Lee, A. F. LoBuglio

Research output: Contribution to journalArticlepeer-review

26 Citations (Scopus)


Platelets from 24 patients with immune thrombocytopenia resistant to standard therapy (refractory ITP), 35 patients with nonimmune thrombocytopenia (non-ITP), and 32 normal donors were studied in regard to platelet surface-bound IgG (PBIgG) and the ability of these platelets to be bound by human monocytes in vitro (monocyte-platelet rosette assay). Fourteen (58%) of the platelet samples from refractory ITP patients but none (0%) from the non-ITP or control donors had PBIgG > 800 molecules IgG/platelet. Seventeen of 24 (71%) of the ITP patients had platelets which demonstrated increased monocyte-platelet rosette formation [rosette index (RI) > 2], whereas only four (11%) of the non-ITP patients had such platelets. There was a direct correlation between PBIgG and rosette index for the platelets from resistant ITP patients. There was no correlation of severity of thrombocytopenia with PBIgG or rosette index. Monocyte-platelet interaction in the presence of elevated PBIgG is mediated through the monocyte Fc-receptor. Platelets from five of ten refractory ITP patients with PBIgG < 800 molecules IgG/platelet had increased rosette formation. Monocyte-platelet interaction in the absence of increased PBIgG may be due to small amounts of platelet surface IgG which are still able to mediate monocyte Fc-receptor interaction or to alternate membrane receptor interaction through the monocyte C3 receptor. Our data underscore the pathophysiologic relevance of monocyte/macrophage-mediated interaction in immune platelet destruction syndromes.

Original languageEnglish
Pages (from-to)1328-1331
Number of pages4
Issue number4
Publication statusPublished - 1989
Externally publishedYes


Dive into the research topics of 'Monocyte-platelet interaction in immune and nonimmune thrombocytopenia'. Together they form a unique fingerprint.

Cite this