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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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NEOPLASIA

Brief Report

PD-1–PD-1 ligand interaction contributes to immunosuppressive microenvironment of Hodgkin lymphoma

Ryo Yamamoto1, Momoko Nishikori1, Toshio Kitawaki1, Tomomi Sakai1, Masakatsu Hishizawa1, Masaharu Tashima1, Tadakazu Kondo1, Katsuyuki Ohmori2, Masayuki Kurata3, Takamasa Hayashi4, and Takashi Uchiyama1

1 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-{gamma}–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.


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