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The effects of STI571 on antigen presentation of dendritic cells generated from patients with chronic myelogenous leukemia
Author(s) -
Sato Naoko,
Narita Miwako,
Takahashi Masuhiro,
Yagisawa Kumiko,
Liu Aichun,
Abe Takashi,
Nikkuni Kohji,
Furukawa Tatsuo,
Toba Ken,
Aizawa Yoshifusa
Publication year - 2003
Publication title -
hematological oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 44
eISSN - 1099-1069
pISSN - 0278-0232
DOI - 10.1002/hon.705
Subject(s) - chronic myelogenous leukemia , cd80 , abl , antigen presentation , tyrosine kinase , biology , breakpoint cluster region , antigen , clone (java method) , imatinib mesylate , cancer research , k562 cells , cytotoxic t cell , cd86 , microbiology and biotechnology , leukemia , immunology , cd40 , imatinib , t cell , immune system , signal transduction , biochemistry , receptor , gene , myeloid leukemia , in vitro
Chronic myelogenous leukemia is caused by the acquisition of the reciprocal (9;22)(q34;q11) chromosomal translocation in hematopoietic stem cells. The fusion protein showed higher and aberrant tyrosine kinase activity. The inhibition of the tyrosine kinase activity of the protein represents a specific therapeutic strategy for bcr/abl‐expressing leukemias. STI571 is a compound of the 2‐phenylaminopyrimidine class that selectively inhibits the tyrosine kinase activity of the Abl protein tyrosine kinase. In this study, we evaluated the effects of STI571 on antigen presentation of dendritic cells generated from the patients with CML. The data showed that by the addition of STI571 the dendritic cells derived from CML clone showed an increased expression of CD1a, CD83, CD80 and CD86 by flow cytometry analysis and showed more intense abilities of allogeneic antigen presentation by mixed leukocyte culture, compared with the control cells without STI571. Our results suggested that STI571 not only has a direct cytotoxic effect on bcr‐abl gene rearranged cells but also an indirect effect associated with increased anti‐leukemic immunological function due to an intensified antigen presentation. Copyright © 2003 John Wiley & Sons, Ltd.