Impaired B cell terminal differentiation in B cell-specific knockout mice of cell death-defying factor anamorsin

Yuri Hamanaka; Akira Tanimura; Takafumi Yokota; Sachiko Ezoe; Michiko Ichii; Yasuhiro Nagate; Kenji Oritani; Yuzuru Kanakura; Naoki Hosen; Hirohiko Shibayama

doi:10.1016/j.bbrc.2022.03.018

Impaired B cell terminal differentiation in B cell-specific knockout mice of cell death-defying factor anamorsin

Biochem Biophys Res Commun. 2022 May 7:603:1-6. doi: 10.1016/j.bbrc.2022.03.018. Epub 2022 Mar 4.

Authors

Affiliations

¹ Department of Hematology and Oncology, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka, 565-0871, Japan.
² Department of Hematology and Oncology, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka, 565-0871, Japan. Electronic address: atanimura@bldon.med.osaka-u.ac.jp.
³ Department of Hematology, National Hospital Organization Osaka National Hospital, 2-1-14 Hoenzaka, Chuo-ku, Osaka, 540-0006, Japan.
⁴ Department of Hematology, Graduate School of Medical Sciences, International University of Health and Welfare, 4-3 Kozunomori, Narita, Chiba, 286-8686, Japan.
⁵ Department of Hematology and Oncology, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka, 565-0871, Japan; Sumitomo Hospital, 5-3-20 Nakanoshima, Kita-ku, Osaka, 530-0005, Japan.
⁶ Department of Hematology and Oncology, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka, 565-0871, Japan; Laboratory of Cellular Immunotherapy, World Premier International Immunology Frontier Research Center, Osaka University, 3-1 Yamada-oka, Suita, Osaka, 565-0871, Japan; Integrated Frontier Research for Medical Science Division, Institute for Open and Transdisciplinary Research Initiatives (OTRI), Osaka University, 2-1 Yamada-oka, Suita, Osaka, 565-0871, Japan.
⁷ Department of Hematology and Oncology, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka, 565-0871, Japan; Department of Hematology, National Hospital Organization Osaka National Hospital, 2-1-14 Hoenzaka, Chuo-ku, Osaka, 540-0006, Japan.

PMID: 35259639
DOI: 10.1016/j.bbrc.2022.03.018

Abstract

Anamorsin (AM) is an anti-apoptotic molecule cloned by us as a molecule that confers resistance against apoptosis induced by growth factor deprivation. AM-deficient mice are embryonic lethal, which impedes detailed analyses of the roles of AM in various types of adult cells. To overcome the embryonic lethality, we generated AM conditional knockout (AM^flox/flox) mice and cell type-specific genetic modification became possible using the Cre-loxP system. CD19-Cre/AM^flox/flox mice with AM deleted specifically in CD19⁺ B cells exhibited less B220⁺ B cells in their spleen, peripheral blood, and lymph node compared with control CD19-Cre mice. Using flow cytometry to categorize bone marrow and spleen cells into B cell subsets, we observed significantly less follicular type I cells, which are the most mature follicular B cells, compared with control CD19-Cre mice. These data suggest that AM has an important role in the generation of mature B cells.

Keywords: Anamorsin; B cell differentiation; Gene knockout; Hematopoiesis; Iron-sulfur prrotein; Lymphocyte.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Animals
Antigens, CD19* / genetics
Apoptosis
B-Lymphocytes*
Cell Differentiation
Mice
Mice, Knockout
Spleen

Substances

Antigens, CD19