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Volume 41, Issue 2, Pages 271-280 (February 2010)


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CD81 protein is expressed at high levels in normal germinal center B cells and in subtypes of human lymphomas

Robert F. Luo, MD, MPHa, Shuchun Zhao, MSa, Robert Tibshirani, PhDb, June H. Myklebust, PhDc, Mrinmoy Sanyal, PhDc, Rosemary Fernandezc, Dita Gratzinger, MD, PhDa, Robert J. Marinelli, PhDd, Zhi Shun Lu, MSa, Anna Wong, MDa, Ronald Levy, MDc, Shoshana Levy, PhDc1, Yasodha Natkunam, MD, PhDaCorresponding Author Information1email address

Received 8 May 2009; received in revised form 28 July 2009; accepted 30 July 2009. published online 09 December 2009.

Summary 

CD81 is a tetraspanin cell surface protein that regulates CD19 expression in B lymphocytes and enables hepatitis C virus infection of human cells. Immunohistologic analysis in normal hematopoietic tissue showed strong staining for CD81 in normal germinal center B cells, a cell type in which its increased expression has not been previously recognized. High-dimensional flow cytometry analysis of normal hematopoietic tissue confirmed that among B- and T-cell subsets, germinal center B cells showed the highest level of CD81 expression. In more than 800 neoplastic tissue samples, its expression was also found in most non-Hodgkin lymphomas. Staining for CD81 was rarely seen in multiple myeloma, Hodgkin lymphoma, or myeloid leukemia. In hierarchical cluster analysis of diffuse large B-cell lymphoma, staining for CD81 was most similar to other germinal center B cell–associated markers, particularly LMO2. By flow cytometry, CD81 was expressed in diffuse large B-cell lymphoma cells independent of the presence or absence of CD10, another germinal center B-cell marker. The detection of CD81 in routine biopsy samples and its differential expression in lymphoma subtypes, particularly diffuse large B-cell lymphoma, warrant further study to assess CD81 expression and its role in the risk stratification of patients with diffuse large B-cell lymphoma.

a Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA

b Department of Health Research and Policy and Statistics, Stanford University School of Medicine, Stanford, CA 94305, USA

c Division of Oncology, Department of Medicine, Division of Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA

d Department of Biochemistry, Stanford University School of Medicine, Stanford, CA 94305, USA

Corresponding Author InformationCorresponding author.

 Support: This work was partly funded by NIH CA34233, CA33399, and the Leukemia and Lymphoma Society SCORE grant. RL is an American Cancer Society Clinical Research Professor and JHM is a Norwegian Cancer Society Fellow.

1 These authors contributed equally.

PII: S0046-8177(09)00285-8

doi:10.1016/j.humpath.2009.07.022


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