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Blood, 15 March 2008, Vol. 111, No. 6, pp. 3220-3224. Prepublished online as a Blood First Edition Paper on January 18, 2008; DOI 10.1182/blood-2007-05-085159.
NEOPLASIA PD-1–PD-1 ligand interaction contributes to immunosuppressive microenvironment of Hodgkin lymphoma1 Department of Hematology and Oncology, Graduate School of Medicine, Kyoto University, Kyoto; 2 Department of Clinical Pathology, Kyoto University Hospital, Shogoin Kawahara-cho, Sakyo-ku, Kyoto; 3 Department of Hematology and Clinical Immunology, Kobe City Medical Center General Hospital, Minatojima-Nakamachi, Chuo-ku, Kobe; and 4 Department of Hematology, Tenri Hospital, Mishima-cho, Tenri, Nara, Japan
Programmed death-1 (PD-1)–PD-1 ligand (PD-L) signaling system is involved in the functional impairment of T cells such as in chronic viral infection or tumor immune evasion. We examined PD-L expression in lymphoid cell lines and found that they were up-regulated on Hodgkin lymphoma (HL) and several T-cell lymphomas but not on B-cell lymphomas. PD-L expression was also demonstrated in primary Hodgkin/Reed-Sternberg (H/RS) cells. On the other hand, PD-1 was elevated markedly in tumor-infiltrating T cells of HL, and was high in the peripheral T cells of HL patients as well. Blockade of the PD-1 signaling pathway inhibited SHP-2 phosphorylation and restored the IFN-
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| Copyright © 2008 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||
–producing function of HL-infiltrating T cells. According to these results, deficient cellular immunity observed in HL patients can be explained by "T-cell exhaustion," which is led by the activation of PD-1–PD-L signaling pathway. Our finding provides a potentially effective immunologic strategy for the treatment of HL. 
