Contribution of BCAP to maintenance of mature B cells through c-Rel

Nat Immunol. 2003 Aug;4(8):780-6. doi: 10.1038/ni949. Epub 2003 Jun 29.

Abstract

Mice deficient in the B cell adaptor for phosphoinositide 3-kinase (BCAP) have reduced numbers of mature B lymphocytes, which show defects in cell survival and proliferation. We found here that the NF-kappa B (Rel) pathway was impaired in BCAP-deficient mature B cells and that NF-kappa B target genes, indispensable for cell survival and division, were not induced in response to B cell receptor (BCR) stimulation. Among the NF-kappa B (Rel) family, expression of c-Rel was specifically reduced in BCAP-deficient B cells. Retrovirus-mediated reintroduction of c-Rel restored the pool size of immunoglobulin (Ig)M(lo)IgD(hi) mature B cells in the spleen as well as proliferative responses to BCR stimulation. These results indicate BCAP is essential in the maintenance of mature B cells through functional coupling with c-Rel.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing*
  • Animals
  • B-Lymphocytes / metabolism*
  • Carrier Proteins / metabolism*
  • Mice
  • NF-kappa B / metabolism*
  • Proto-Oncogene Proteins c-rel / metabolism*

Substances

  • Adaptor Proteins, Signal Transducing
  • Carrier Proteins
  • NF-kappa B
  • Pik3ap1 protein, mouse
  • Proto-Oncogene Proteins c-rel