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Protein kinase Cδ controls self-antigen-induced B-cell tolerance

Author

Listed:
  • Ingrid Mecklenbräuker

    (The Rockefeller University)

  • Kaoru Saijo

    (The Rockefeller University)

  • Nai-Ying Zheng

    (The Rockefeller University)

  • Michael Leitges

    (Max Planck Institute for Experimental Endocrinology)

  • Alexander Tarakhovsky

    (The Rockefeller University)

Abstract

Interaction of a B cell expressing self-specific B-cell antigen receptor (BCR) with an auto-antigen results in either clonal deletion or functional inactivation1,2,3. Both of these processes lead to B-cell tolerance and are essential for the prevention of auto-immune diseases. Whereas clonal deletion results in the death of developing autoreactive B cells, functional inactivation of self-reactive B lymphocytes leads to complex changes in the phenotype of peripheral B cells, described collectively as anergy1,2,3. Here we demonstrate that deficiency in protein kinase Cδ (PKC-δ) prevents B-cell tolerance, and allows maturation and terminal differentiation of self-reactive B cells in the presence of the tolerizing antigen. The importance of PKC-δ in B-cell tolerance is further underscored by the appearance of autoreactive anti-DNA and anti-nuclear antibodies in the serum of PKC-δ-deficient mice. As deficiency of PKC-δ does not affect BCR-mediated B-cell activation in vitro and in vivo, our data suggest a selective and essential role of PKC-δ in tolerogenic, but not immunogenic, B-cell responses.

Suggested Citation

  • Ingrid Mecklenbräuker & Kaoru Saijo & Nai-Ying Zheng & Michael Leitges & Alexander Tarakhovsky, 2002. "Protein kinase Cδ controls self-antigen-induced B-cell tolerance," Nature, Nature, vol. 416(6883), pages 860-865, April.
  • Handle: RePEc:nat:nature:v:416:y:2002:i:6883:d:10.1038_416860a
    DOI: 10.1038/416860a
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