title: Frequent reversible membrane damage in peripheral blood B cells in human T cell lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP).
abstract: Apoptosis in peripheral blood lymphocyte populations in HTLV-I-infected people in vivo was examined, to study the lymphocyte dynamics in HTLV-I infection. Freshly isolated lymphocytes from 10 non-infected healthy people, eight asymptomatic HTLV-I carriers and 15 patients with HAM/TSP were stained with FITC-labelled annexin V to detect phosphatidylserine (PS) residue exposure at the outer plasma membrane leaflet as an early marker of apoptosis. There was no significant difference in annexin V positivity in CD4+ and CD8+ lymphocytes between non-infected subjects, asymptomatic carriers and HAM/TSP patients, but there was a greatly increased exposure of PS on CD19+ lymphocytes (B cells) detected by FITC-annexin V in 12 out of 15 (80%) HAM/TSP patients, while only two out of eight (25%) asymptomatic carriers and none of the non-infected healthy people showed this aberrant PS exposure on B cells. The intensity of annexin V staining of B cells in HAM/TSP was intermediate, as distinct from the high annexin V staining on advanced apoptotic cells. However, annexin V positivity was decreased when the cells were stained after 24 h of culture, suggesting that the intermediate PS exposure on the B cell in HAM/TSP is not a consequence of an apoptotic process, but rather reflects reversible membrane damage. B cells with PS exposure in vivo might provide a site for coagulation and inflammation, and so contribute to the pathogenesis of HAM/TSP and its complications.
authors.affiliation: Department of Immunology, Imperial College School of Medicine at St Mary's, London, UK.
authors.forename: Y
authors.initials: Y
authors.lastname: Furukawa
authors.forename: C R
authors.initials: CR
authors.lastname: Bangham
authors.forename: G P
authors.initials: GP
authors.lastname: Taylor
authors.forename: J N
authors.initials: JN
authors.lastname: Weber
authors.forename: M
authors.initials: M
authors.lastname: Osame
mesh_terms: D000328:Adult; D017304:Annexin A5 / Q000276:immunology; D017153:Antibodies, Anticardiolipin / Q000276:immunology; D018941:Antigens, CD19 / Q000276:immunology; D017209:Apoptosis / Q000276:immunology*; D001402:B-Lymphocytes / Q000166:cytology / Q000276:immunology*; D015415:Biomarkers; D053148:Caspase 3; D020169:Caspases / Q000378:metabolism; D002462:Cell Membrane / Q000473:pathology; D002478:Cells, Cultured; D004789:Enzyme Activation; D006023:Glycoproteins / Q000276:immunology; D015368:Human T-lymphotropic virus 1 / Q000235:genetics / Q000276:immunology*; D006801:Humans; D015493:Paraparesis, Tropical Spastic / Q000097:blood / Q000276:immunology*; D013194:Staining and Labeling / Q000379:methods; D013997:Time Factors; D019562:Viral Load; D053482:beta 2-Glycoprotein I; D019014:fas Receptor / Q000276:immunology
chemical_list: D017304:Annexin A5; D017153:Antibodies, Anticardiolipin; D018941:Antigens, CD19; D015415:Biomarkers; D006023:Glycoproteins; D053482:beta 2-Glycoprotein I; D019014:fas Receptor; C505407:CASP3 protein, human; D053148:Caspase 3; D020169:Caspases