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 Blood, 3 September 2009, Vol. 114, No. 10, pp. 2149-2158.
Prepublished online as a Blood First Edition Paper on July 13, 2009; DOI 10.1182/blood-2009-04-216671.

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LYMPHOID NEOPLASIA

B7-H1 (PD-L1, CD274) suppresses host immunity in T-cell lymphoproliferative disorders

Ryan A. Wilcox1, Andrew L. Feldman2, David A. Wada3, Zhi-Zhang Yang1, Nneka I. Comfere3, Haidong Dong4, Eugene D. Kwon5, Anne J. Novak1, Svetomir N. Markovic1, Mark R. Pittelkow3, Thomas E. Witzig1, and Stephen M. Ansell1

1 Division of Hematology and Departments of 2 Laboratory Medicine and Pathology, 3 Dermatology, 4 Immunology, and 5 Urology, Mayo Clinic, Rochester, MN

Stromal elements present within the tumor microenvironment may suppress host immunity and promote the growth of malignant lymphocytes in B cell–derived non-Hodgkin lymphoma (NHL). In contrast, little is known about the microenvironment's role in T cell–derived NHL. B7-H1 (PD-L1, CD274), a member of the B7 family of costimulatory/coinhibitory ligands expressed by both malignant cells and stromal cells within the tumor microenvironment, has emerged as an important immune modulator capable of suppressing host immunity. Therefore, B7-H1 expression and function were analyzed in cutaneous and peripheral T-cell NHL. B7-H1 was expressed by tumor cells, monocytes, and monocyte-derived cells within the tumor microenvironment in T-cell NHL and was found to inhibit T-cell proliferation and promote the induction of FoxP3+ regulatory T cells. Collectively, the data presented provide the first evidence implicating B7-H1 in the suppression of host immunity in T-cell lymphoproliferative disorders and suggest that the targeting of B7-H1 may represent a novel therapeutic approach.


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