Seroreactivity to LGL leukemia-specific epitopes in aplastic anemia, myelodysplastic syndrome and paroxysmal nocturnal hemoglobinuria: Results of a bone marrow failure consortium study

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• 作者：Susan Bell Nyland^a ; ^{snyland@hmc.psu.edu} ; Daniel J. Krissinger^a ; Michael J. Clemente^b ; Rosalyn B. Irby^a ; Kendall Thomas Baab^a ; Nancy Ruth Jarbadan^a ; Lubomir Sokol^c ; Eric Schaefer^d ; Jason Liao^d ; David Cuthbertson^e ; Pearlie Epling-Burnette^c ; ^f ; Ronald Paquette^g ; Alan F. List^c ; Jaroslaw P. Maciejewski^b ; Thomas P. Loughran Jr.^a
• 关键词：LGL leukemia ; Aplastic anemia ; Myelodysplastic syndrome ; Paroxysmal nocturnal hemoglobinuria ; HTLV antibody
• 刊名：Leukemia Research
• 出版年：2012
• 期刊代码：186_01452126
• 类别：med
• 出版时间：May, 2012
• 卷：36
• 期：5
• 页码：581-587
• 文件大小：563 K

摘要

Large granular lymphocyte (LGL) leukemia is characterized by clonal expansion of antigen-activated cytotoxic T cells (CTL). Patients frequently exhibit seroreactivity against a human T-cell leukemia virus (HTLV) epitope, BA21. Aplastic anemia, paroxysmal nocturnal hemoglobinuria and myelodysplastic syndrome are bone marrow failure diseases that can also be associated with similar aberrant CTL activation (LGL-BMF). We identified a BA21 peptide that was specifically reactive with LGL leukemia sera and found significantly elevated antibody reactivity against the same peptide in LGL-BMF sera. This finding of shared seroreactivity in LGL-BMF conditions and LGL leukemia suggests that these diseases might share a common pathogenesis.