Comparison of platelet immunity in patients with SLE and with ITP

• Published in: Transfusion science Vol. 22; no. 1; pp. 19 - 27
• Main Authors: Lazarus, Alan H, Ellis, Janet, Semple, John W, Mody, Meera, Crow, Andrew R, Freedman, John
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.02.2000
• Subjects: Adult; Antigen-Presenting Cells - cytology; Blood Platelets - cytology; Blood Platelets - immunology; Cell Division - drug effects; Cytokines; Cytokines - blood; Cytological Techniques; Humans; Idiopathic thrombocytopenic purpura; Immunity; Lupus Erythematosus, Systemic - blood; Lupus Erythematosus, Systemic - immunology; Lymphocyte Activation; Lymphocytes - cytology; Lymphocytes - drug effects; Lymphocytes - immunology; Mitogens - pharmacology; Platelet Count; Platelet Function Tests; Platelets; Purpura, Thrombocytopenic, Idiopathic - blood; Purpura, Thrombocytopenic, Idiopathic - immunology; Systemic lupus erythematosus; Idiopathic thrombocytopenic purpura; Systemic lupus erythematosus; Cytokines; Platelets
• ISSN: 0955-3886; 1879-3126
• DOI: 10.1016/S0955-3886(00)00004-7

Idiopathic thrombocytopenic purpura (ITP) is characterized by the development of a specific anti-platelet autoantibody immune response mediating the development of thrombocytopenia. Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the production of a wide variety of autoantibodies. In 15–20% of SLE cases, patients develop thrombocytopenia which appears to be autoimmune in nature (SLE-TP). To better understand the pathogenesis of the thrombocytopenia associated with SLE, we investigated the overlapping platelet and cellular immune features between SLE and ITP. Thirty-one patients with SLE, eight with SLE-TP, and 17 with ITP, were studied and compared to 60 healthy controls. We evaluated platelet-associated IgG, platelet microparticles, reticulated platelets, platelet HLA-DR expression, in vivo cytokine levels, lymphocyte proliferation, and the T lymphocyte anti-platelet immune response in these patients. Patients with SLE-TP and those with ITP had increased platelet-associated IgG, an increased percentage of platelet microparticles, a higher percentage of reticulated platelets and larger platelets, suggesting antibody-mediated platelet destruction and increased platelet production. More than 50% of patients with ITP had increased HLA-DR on their platelet surface whereas subjects with SLE-TP did not. Analysis of serum cytokines demonstrated increased levels of IL-10, IL-15 and TNF- α in patients with SLE, but in those with ITP, only increased levels of IL-15 were seen, no increases in any of these cytokines were observed in patients with in SLE-TP. The ability of lymphocytes to proliferate in response to phorbol myristate acetate (PMA) stimulation was increased in SLE-TP, but was normal in both SLE and ITP. Lymphocytes from subjects with ITP displayed an increased ability to proliferate on exposure to platelets, in contrast, those with SLE-TP did not. While the number of subjects evaluated with SLE-TP was small, these data reveal a number of differences in the immunopathogenesis between SLE-TP and ITP.