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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.
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Submitted May 1, 2007
Accepted January 11, 2008
PD-1-PD-1-ligand interaction contributes to immunosuppressive microenvironment of Hodgkin lymphoma
Ryo Yamamoto, Momoko Nishikori*, Toshio Kitawaki, Tomomi Sakai, Masakatsu Hishizawa, Masaharu Tashima, Tadakazu Kondo, Katsuyuki Ohmori, Masayuki Kurata, Takamasa Hayashi, and Takashi Uchiyama
Department of Hematology and Oncology, Graduate School of Medicine, Kyoto University, Kyoto, Japan
Department of Clinical Pathology, Kyoto University Hospital, Kyoto, Japan
Department of Hematology and Clinical Immunology, Kobe City Medical Center General Hospital, Kobe, Japan
Department of Hematology, Tenri Hospital, Tenri, Japan
* Corresponding author; email: nishikor{at}kuhp.kyoto-u.ac.jp.
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 upregulated 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- 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 immunological strategy for the treatment of HL.
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