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Blood, 1 February 2004, Vol. 103, No. 3, pp. 1002-1010.
Prepublished online as a Blood First Edition Paper on October 2, 2003; DOI 10.1182/blood-2003-08-2691.
Submitted August 8, 2003
Accepted September 23, 2003
Association of CD26 with CD45RA outside lipid rafts attenuates cord blood T-cell activation
Seiji Kobayashi, Kei Ohnuma, Masahiko Uchiyama, Kouichi Iino, Satoshi Iwata, Nam H Dang, and Chikao Morimoto*
Advanced Clinical Research Center, Institute of Medical Science, Division of Clinical Immunology, University of Tokyo, Tokyo, Japan; Department of Lymphoma/Myeloma, University of Texas M. D. Anderson Cancer Center, Houston, TX, USA
* Corresponding author; email: morimoto{at}ims.u-tokyo.ac.jp.
CD26 is a T-cell activation antigen that contains dipeptidyl peptidase IV activity and binds adenosine deaminase. Recent work showed that specialized membrane microdomains, also known as lipid rafts, play a key role in T-cell signaling. In this study, we investigate the role of CD26 in cord blood T-cell activation and signal transduction. We demonstrated that different expression levels of CD26 were observed between cord blood T cells (CBTCs) and peripheral T cells (PBTCs), and that CD26+CD45RA+ CBTCs were different as compared with CD26+CD45RA+ PBTCs. Moreover, the comitogenic effect of CD26 was not as pronounced in CBTCs as in PBTCs. We also showed that CD26 crosslinking induced less phosphorylation of T-cell receptor signaling molecules Lck, ZAP-70, TCR- , and LAT in CBTCs than in PBTCs. Furthermore, CD26 molecules associated with CD45RA molecules outside lipid rafts in CBTCs. Our results suggest that strong physical linkage of CD26 with CD45RA outside lipid rafts may be responsible for the attenuation of T-cell activation signaling through CD26, which may be responsible for immature immune response and the low incidence of severe graft-versus-host disease in cord blood transplantation.
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