Self-reactive B lymphocytes overexpressing Bcl-xL escape negative selection and are tolerized by clonal anergy and receptor editing

Immunity. 1998 Jul;9(1):35-45. doi: 10.1016/s1074-7613(00)80586-5.


Self-reactive B cells Tg for both a bcl-xL death inhibitory gene and an Ig receptor recognizing hen egg lysozyme (HEL-Ig) efficiently escaped developmental arrest and deletion in mice expressing membrane-bound self-antigen (mHEL). In response to the same antigen, Tg HEL-Ig B cells not expressing bcl-xL were deleted, while cells expressing bcl-2 were arrested at the immature B stage. Bcl-xL Tg B cells escaping negative selection were anergic in both in vitro and in vivo assays and showed some evidence for receptor editing. These studies suggest that Bcl-x may have a distinct role in controlling survival at the immature stage of B cell development and demonstrate that tolerance is preserved when self-reactive B cells escape central deletion.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Apoptosis*
  • B-Lymphocytes / immunology*
  • B-Lymphocytes / metabolism
  • Chimera
  • Clonal Anergy / immunology*
  • DNA-Binding Proteins / genetics
  • Female
  • Homeodomain Proteins / genetics
  • Leukopoiesis
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Proto-Oncogene Proteins c-bcl-2 / biosynthesis
  • Proto-Oncogene Proteins c-bcl-2 / genetics
  • Proto-Oncogene Proteins c-bcl-2 / physiology*
  • Receptors, Antigen, B-Cell / metabolism*
  • Transgenes
  • bcl-X Protein


  • Bcl2l1 protein, mouse
  • DNA-Binding Proteins
  • Homeodomain Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • Rag2 protein, mouse
  • Receptors, Antigen, B-Cell
  • V(D)J recombination activating protein 2
  • bcl-X Protein
  • RAG-1 protein