title: Comparison of platelet immunity in patients with SLE and with ITP.
abstract: 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-alpha 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.
authors.affiliation: Division of Immunohaematology, St Michael's Hospital, Toronto, Ont., Canada. lazarusa@smh.toronto.on.ca
authors.forename: A H
authors.initials: AH
authors.lastname: Lazarus
authors.forename: J
authors.initials: J
authors.lastname: Ellis
authors.forename: J W
authors.initials: JW
authors.lastname: Semple
authors.forename: M
authors.initials: M
authors.lastname: Mody
authors.forename: A R
authors.initials: AR
authors.lastname: Crow
authors.forename: J
authors.initials: J
authors.lastname: Freedman
mesh_terms: D000328:Adult; D000938:Antigen-Presenting Cells / Q000166:cytology; D001792:Blood Platelets / Q000166:cytology / Q000276:immunology*; D002455:Cell Division / Q000187:drug effects; D016207:Cytokines / Q000097:blood; D003584:Cytological Techniques; D006801:Humans; D007109:Immunity; D008180:Lupus Erythematosus, Systemic / Q000097:blood* / Q000276:immunology; D008213:Lymphocyte Activation; D008214:Lymphocytes / Q000166:cytology / Q000187:drug effects / Q000276:immunology; D008934:Mitogens / Q000494:pharmacology; D010976:Platelet Count; D010979:Platelet Function Tests; D016553:Purpura, Thrombocytopenic, Idiopathic / Q000097:blood* / Q000276:immunology
chemical_list: D016207:Cytokines; D008934:Mitogens