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

Ingrid Mecklenbräuker, Kaoru Saijo, Nai-Ying Zheng, Michael Leitges and Alexander Tarakhovsky ()
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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

Nature, 2002, vol. 416, issue 6883, 860-865

Abstract: 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.

Date: 2002
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DOI: 10.1038/416860a

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