4.2 Article

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

Journal

HUMAN IMMUNOLOGY
Volume 72, Issue 10, Pages 798-804

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.humimm.2011.06.015

Keywords

CDR3 structure; Leukemia; T cell repertoire; T cell receptor (TCR) V beta gene

Categories

Funding

  1. National 863 Project [2006AA02Z114]
  2. National Natural Science Foundation of China [39870358]
  3. Natural Science Foundation of Guangdong Province, China [05103293, 9251063201000001]

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The clonally expanded T cells identified in most cancer patients that respond to tumor-associated antigen such as P210(BCR-ABL) protein have definite, specific antitumor cytotoxicity. T cell receptor (TCR) V beta 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 V beta 21 subfamily was observed in the peripheral blood of CML and B-ALL patients. These clonally expanded V beta 21 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 J beta 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 J beta 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 V beta 21 subfamily expansion in p210(BCR-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 V beta 21 T cell clones were derived from the stimulation of p210(BCR-ABL) protein. (C) 2011 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved.

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