کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3350698 1216404 2011 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Characterization of the CDR3 structure of the Vβ21 T cell clone in patients with P210BCR-ABL-positive chronic myeloid leukemia and B-cell acute lymphoblastic leukemia
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی ایمونولوژی
پیش نمایش صفحه اول مقاله
Characterization of the CDR3 structure of the Vβ21 T cell clone in patients with P210BCR-ABL-positive chronic myeloid leukemia and B-cell acute lymphoblastic leukemia
چکیده انگلیسی

The clonally expanded T cells identified in most cancer patients that respond to tumor-associated antigen such as P210BCR-ABL protein have definite, specific antitumor cytotoxicity. T cell receptor (TCR) Vβ CDR3 repertoire diversity was analyzed in patients with chronic myeloid leukemia (CML) and BCR-ABL+ B-cell acute lymphoblastic leukemia (B-ALL) by GeneScan. A high frequency of oligoclonal expansion of the TCR Vβ21 subfamily was observed in the peripheral blood of CML and B-ALL patients. These clonally expanded Vβ21 T cells were correlated with the pathophysiologic process of CML. A conserved amino acid motif (SLxxV) was observed within the CDR3 region in only 3 patients with CML. Preferential usage of the Jβ segments was also observed in a minority of patients. The 3-dimensional structures of the CDR3 region containing the same motif or using the same Jβ segment displayed low similarity; on the contrary, the conformation of the CDR3 region containing no conserved motif in some T cell clones was highly similar. In conclusion, our findings indicate a high frequency of TCR Vβ21 subfamily expansion in p210BCR-ABL-positive CML and B-ALL patients. The characterization of the CDR3 structure was complex. Regrettably, at this time it was not possible to confirm that the Vβ21 T cell clones were derived from the stimulation of p210BCR-ABL protein.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Human Immunology - Volume 72, Issue 10, October 2011, Pages 798–804
نویسندگان
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