Mice Deficient in Nuclear Factor (NF)-κB/p52 Present with Defects in Humoral Responses, Germinal Center Reactions, and Splenic Microarchitecture

• DOI: 10.1084/jem.187.2.147
• Publication Date: 2002-07-26T16:49:30Z
• Authors: Guido Franzoso; Louise Carlson; Ljiljana Poljak; Elizabeth W. Shores; Suzanne Epstein; Antonio Leonardi; Alex Grinberg; Tom Tran; Tanya Scharton-Ke...; Miriam Anver; Paul Love; Keith Brown; Ulrich Siebenlist
• Keywords: Mice, Knockout; 0301 basic medicine; B-Lymphocyte Subsets; Immunologic Deficiency Syndromes; NF-kappa B; Mice, Inbred Strains; Germinal Center; Adoptive Transfer; Mice; 03 medical and health sciences; Toxoplasmosis, Animal; T-Lymphocyte Subsets; Proto-Oncogene Proteins; Antibody Formation; Animals; Lymphocyte Count; Toxoplasma; Spleen

p52 is a subunit of nuclear factor (NF)-kappa B transcription factors, most closely related to p50. Previously, we have shown that p52, but not p50 homodimers can form transactivating complexes when associated with Bcl-3, an unusual member the I kappa family. To determine nonredundant physiologic roles generated mice deficient in p52. Null mutant were impaired their ability generate antibodies T-dependent antigens, consistent absence cell follicles and follicular dendritic networks secondary lymphoid organs, inability germinal centers. Furthermore, splenic marginal zone was disrupted. These phenotypes are largely overlapping those observed Bcl-3 knockout animals, distinct from knockouts, supporting notion physiologically relevant complex Bcl-3. Adoptive transfer experiments further suggest such may be critical accessory functions during antigen-specific immune reactions. Possible discussed underlie oncogenic potential these proteins, as evidenced by recurrent chromosomal translocations genes tumors.