The roles of BST‐2 in murine B cell development and on virus propagation

Author:

Urata Shuzo12ORCID,Yamaguchi Sachiko34,Nambu Aya3,Sudo Katsuko5,Nakae Susumu346,Yasuda Jiro127

Affiliation:

1. Department of Emerging Infectious Diseases, Institute of Tropical Medicine (NEKKEN) Nagasaki University Nagasaki Japan

2. National Research Center for the Control and Prevention of Infectious Diseases (CCPID) Nagasaki University Nagasaki Japan

3. Laboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science The University of Tokyo Tokyo Japan

4. Graduate School of Integrated Sciences for Life Hiroshima University Hiroshima Japan

5. Pre‐clinical Research Center Tokyo Medical University Tokyo Japan

6. Precursory Research for Embryonic Science and Technology (PRESTO), Japan Science and Technology Agency Saitama Japan

7. Program for Nurturing Global Leaders in Tropical and Emerging Communicable Diseases, Graduate School of Biomedical Sciences Nagasaki University Nagasaki Japan

Abstract

AbstractThe bone marrow (BM) stromal cell antigen‐2 (BST‐2), also known as tetherin, CD317, PDCA‐1, or HM1.24, is a membrane protein overexpressed in several types of tumors and may act as a promising target for cancer treatment via antibody‐dependent cellular cytotoxicity. BST‐2 is also expressed in human BM stromal cells (BMSC), which support B cell development. While the activity of BST‐2 as an antiviral factor has been demonstrated, the expression patterns and the role of BST‐2 on B‐cell development and activation have not been investigated, especially in vivo. In this study, Bst2 knockout (Bst2−/−) mice were generated to assess the role of BST‐2 on B cell development and activation. It was observed that BST‐2 was not expressed in BMSC or all B cell progenitors even in wild‐type mice and does not play a significant role in B cell development. In addition, the loss of BST‐2 had no effect on B cell activation. Furthermore and in contrast to the well‐known antiviral role of BST‐2, infection of vesicular stomatitis Indiana virus to the BM cells collected from the Bst2−/− mice produced less infectious virus compared with that from the WT mice. These results suggest that murine BST‐2 is different from human BST‐2 in the expression pattern, physiological function, in vivo, and might possess positive role on VSV replication.

Publisher

Wiley

Subject

Virology,Immunology,Microbiology

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