PMID- 10586052
OWN - NLM
STAT- MEDLINE
DCOM- 20000106
LR  - 20191210
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 163
IP  - 12
DP  - 1999 Dec 15
TI  - Distinct activities of p52/NF-kappa B required for proper secondary lymphoid
      organ microarchitecture: functions enhanced by Bcl-3.
PG  - 6581-8
AB  - Mice rendered deficient in p52, a subunit of NF-kappa B, or in Bcl-3, an I kappa 
      B-related regulator that associates with p52 homodimers, share defects in the
      microarchitecture of secondary lymphoid organs. The mutant mice are impaired in
      formation of B cell follicles and are unable to form proper follicular dendritic 
      cell (FDC) networks upon antigenic challenge. The defects in formation of B cell 
      follicles may be attributed, at least in part, to impaired production of the B
      lymphocyte chemoattractant (BLC) chemokine, possibly a result of defective FDCs. 
      The p52- and Bcl-3-deficient mice exhibit additional defects within the splenic
      marginal zone, including reduced numbers of metallophilic macrophages, reduced
      deposition of the laminin-beta 2 chain and impaired expression of a mucosal
      addressin marker on sinus-lining cells. Whereas p52-deficient mice are severely
      defective in all of these aspects, Bcl-3-deficient mice are only partially
      defective. We determined that FDCs or other non-hemopoietic cells that underlie
      FDCs are intrinsically impaired in p52-deficient mice. Adoptive transfers of
      wild-type bone marrow into p52-deficient mice failed to restore FDC networks or
      follicles. The transfers did restore metallophilic macrophages to the marginal
      zone, however. Together, the results suggest that p52 carries out functions
      essential for a proper splenic microarchitecture in both hemopoietic and
      non-hemopoietic cells and that Bcl-3 is important in enhancing these essential
      activities of p52.
FAU - Poljak, L
AU  - Poljak L
AD  - Laboratory of Immunoregulation, National Institute of Allergy and Infectious
      Diseases, Bethesda, MD 20892, USA.
FAU - Carlson, L
AU  - Carlson L
FAU - Cunningham, K
AU  - Cunningham K
FAU - Kosco-Vilbois, M H
AU  - Kosco-Vilbois MH
FAU - Siebenlist, U
AU  - Siebenlist U
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Adjuvants, Immunologic)
RN  - 0 (Antigen-Antibody Complex)
RN  - 0 (B-Cell Lymphoma 3 Protein)
RN  - 0 (Bcl3 protein, mouse)
RN  - 0 (Chemokine CXCL13)
RN  - 0 (Chemokines, CXC)
RN  - 0 (Cxcl13 protein, mouse)
RN  - 0 (NF-kappa B)
RN  - 0 (NF-kappa B p50 Subunit)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (Transcription Factors)
SB  - IM
MH  - Adjuvants, Immunologic/genetics/*physiology
MH  - Adoptive Transfer
MH  - Animals
MH  - Antigen-Antibody Complex/immunology
MH  - B-Cell Lymphoma 3 Protein
MH  - Basement Membrane/immunology/pathology
MH  - Bone Marrow Transplantation/immunology/pathology
MH  - Chemokine CXCL13
MH  - Chemokines, CXC/biosynthesis/genetics
MH  - Dendritic Cells, Follicular/immunology/metabolism/pathology
MH  - Gene Expression Regulation/immunology
MH  - Lymphoid Tissue/*cytology/*immunology/pathology
MH  - Macrophages/cytology/immunology
MH  - Mice
MH  - Mice, Knockout
MH  - NF-kappa B/biosynthesis/deficiency/genetics/*physiology
MH  - NF-kappa B p50 Subunit
MH  - Proto-Oncogene Proteins/biosynthesis/genetics/*physiology
MH  - Spleen/immunology/metabolism/pathology
MH  - Transcription Factors
MH  - Transcription, Genetic/immunology
EDAT- 1999/12/10 00:00
MHDA- 1999/12/10 00:01
CRDT- 1999/12/10 00:00
PHST- 1999/12/10 00:00 [pubmed]
PHST- 1999/12/10 00:01 [medline]
PHST- 1999/12/10 00:00 [entrez]
AID - ji_v163n12p6581 [pii]
PST - ppublish
SO  - J Immunol. 1999 Dec 15;163(12):6581-8.