title: Plasma-soluble Fas (APO-1, CD95) and soluble Fas ligand in immune thrombocytopenic purpura.
abstract: We investigated the levels of various cytokines and soluble factors in ITP patients, in order to determine the influence of these factors on the pathogenesis of ITP. We found increases in IL-2, IL-6, IFN-gamma, and M-CSF levels in ITP patients compared with those in healthy individuals. On lymphocyte phenotype analysis, we found no clear difference in total T cell population (CD2+ CD19- cells) or cytotoxic T cell frequency (CD8+ CD11b- cells) between these two groups. The frequency of helper/inducer T cells (CD4+ CD8- cells) was decreased in ITP patients. There was a significant increase in activated T cells (CD3+ HLA-DR+ cells) in ITP patients. Furthermore, frequencies of NK cells of potent activity (CD16+ CD56+ cells) were significantly elevated in ITP patients. Seventeen of the 54 ITP patients (31.5%) had elevated levels of sFas, and 11 of the 54 patients (20.4%) of sFasL. In addition, a significant increase of sFasL was observed in sFas-positive ITP patients, and in these patients the sFasL level was correlated with that of sFas (r = 0.687, p < 0.01). We found significant increases in IL-2 and sIL-2R levels in sFas-positive ITP patients. For other factors examined, however, there were no differences in level between sFas-positive and -negative ITP patients. Percentages of activated T cells (CD3+ and HLA-DR+ cells) and NK cells (CD16+ and CD56+ cells) were significantly higher in sFas-positive ITP patients than in sFas-negative ITP patients. These findings suggests that the pathogenesis of ITP includes alteration of the Fas/FasL pathway.
authors.affiliation: First Department of Internal Medicine, Kansai Medical University, Moriguchi, Osaka, Japan.
authors.forename: C
authors.initials: C
authors.lastname: Yoshimura
authors.forename: S
authors.initials: S
authors.lastname: Nomura
authors.forename: M
authors.initials: M
authors.lastname: Nagahama
authors.forename: Y
authors.initials: Y
authors.lastname: Ozaki
authors.forename: H
authors.initials: H
authors.lastname: Kagawa
authors.forename: S
authors.initials: S
authors.lastname: Fukuhara
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000276:immunology; D053222:Fas Ligand Protein; D005260:Female; D006801:Humans; D016130:Immunophenotyping; D008297:Male; D008562:Membrane Glycoproteins / Q000097:blood*; D008875:Middle Aged; D011696:Purpura, Thrombocytopenic / Q000097:blood* / Q000209:etiology / Q000276:immunology*; D016176:T-Lymphocyte Subsets / Q000276:immunology; D019014:fas Receptor / Q000097:blood*
chemical_list: D015703:Antigens, CD; C505661:FASLG protein, human; D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins; D019014:fas Receptor