| First Author | Mecklenbräuker I | Year | 2002 |
| Journal | Nature | Volume | 416 |
| Issue | 6883 | Pages | 860-5 |
| PubMed ID | 11976686 | Mgi Jnum | J:76134 |
| Mgi Id | MGI:2178700 | Doi | 10.1038/416860a |
| Citation | Mecklenbrauker I, et al. (2002) Protein kinase Cdelta controls self-antigen-induced B-cell tolerance. Nature 416(6883):860-5 |
| abstractText | Interaction of a B cell expressing self-specific B-cell antigen receptor (BCR) with an auto-antigen results in either clonal deletion or functional inactivation. 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 anergy. Here we demonstrate that deficiency in protein kinase Cdelta (PKC-delta) 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-delta in B-cell tolerance is further underscored by the appearance of autoreactive anti-DNA and anti-nuclear antibodies in the serum of PKC-delta-deficient mice. As deficiency of PKC-delta does not affect BCR-mediated B-cell activation in vitro and in vivo, our data suggest a selective and essential role of PKC-delta in tolerogenic, but not immunogenic, B-cell responses. |
