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

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Abstract

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 ofBCRs in peripheral B cells.

Journal

  • Memoirs of the Faculty of Engineering, Okayama University

    Memoirs of the Faculty of Engineering, Okayama University 36(2), 51-60, 2002-03

    Faculty of Engineering, Okayama University

Codes

  • NII Article ID (NAID)
    80015582223
  • NII NACSIS-CAT ID (NCID)
    AA10699856
  • Text Lang
    ENG
  • Article Type
    departmental bulletin paper
  • ISSN
    0475-0071
  • Data Source
    IR 
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