Memoirs of the Faculty of Engineering, Okayama University
Published by Faculty of Enginerring, Okayama University

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Memoirs of the School of Engineering, Okayama University

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Regulatory Role for Complement Receptors (CD21/CD35) in the Recombination Activating Gene Expression in Mouse Peripheral B Cells

Hikida, Masaki Department of Bioscience and Biotechnology, Faculty of Engineering, Okayama University
Magari, Masaki Department of Bioscience and Biotechnology, Faculty of Engineering, Okayama University
Nakayama, Yasunori Department of Bioscience and Biotechnology, Faculty of Engineering, Okayama University
Kanayama, Naoki Department of Bioscience and Biotechnology, Faculty of Engineering, Okayama University
Ohmori, Hitoshi Department of Bioscience and Biotechnology, Faculty of Engineering, Okayama University
抄録
A population of peripheral B cells have been shown to express recombination activating gene products, RAG-1 and RAG-2, which are considered to be involved in revising the B cell antigen receptor (BCR) in the periphery. BCR engagement has been reported to turn off RAG expression in peripheral B cells, whereas the same treatment has an opposite effect in immature B cells in the bone marrow. In contrast to receptor editing that is involved in the removal of autoreactivity in immature B cells, it has been shown that secondary V(D)J rearrangement in peripheral B cells, termed receptor revision, contributes to affinity maturation of antibodies. Here, we show that RAG-2 expression in murine splenic B cells was abrogated by the coligation of BCR with complement receptors (CD21/CD35) much more efficiently than by the engagement of BCR alone. On the other hand, the same coligation augmented proliferation of anti-CD40-stimulated B cells. Consistent with these observations, RAG-2 expression was lower in the draining lymph nodes of the quasi-monoclonal mice when they were immunized with a high-affinity antigen than with a low-affinity one. These findings suggest a crucial role for CD21/CD35 in directing the conservation or the revision of BCRs in peripheral B cells.
ISSN
0475-0071
NCID
AA10699856