Pregled bibliografske jedinice broj: 256032
Activities of p52/NF-kB Required for Proper Secondary Lymphoid Organ Microarchitecture: Functions Enhanced by Bcl-3
Activities of p52/NF-kB Required for Proper Secondary Lymphoid Organ Microarchitecture: Functions Enhanced by Bcl-3 // Journal of Immunology, 163 (1999), 6581-6588 (međunarodna recenzija, članak, znanstveni)
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Naslov
Activities of p52/NF-kB Required for Proper Secondary Lymphoid Organ Microarchitecture: Functions Enhanced by Bcl-3
(Distinct Activities of p52/NF-kB required for Proper Secondary Lymphoid Organ Microarchitecture: Functions Enhanced by Bcl-3)
Autori
Poljak, Ljiljana ; Carlson, Louise ; Cunningham Kirk ; Kosco-Vilbois, Marie ; Siebenlist, Ulrich
Izvornik
Journal of Immunology (0022-1767) 163
(1999);
6581-6588
Vrsta, podvrsta i kategorija rada
Radovi u časopisima, članak, znanstveni
Ključne riječi
NF-kB transcription factor; chemokines; extracellular matrix; p52 knockout mice
Sažetak
Mice rendered deficient in p52, a subunit of NF-kB, or Bcl-3, a an IkB-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 follicluar 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 B2 chain and impaired expression of a muocasal 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-deficeint mice. Adoptive transfers of wild-type bone marrow into p52-deficient mice failed to restore FDC networks or follicles. The transfer 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.
Izvorni jezik
Engleski
Znanstvena područja
Temeljne medicinske znanosti
POVEZANOST RADA
Citiraj ovu publikaciju:
Časopis indeksira:
- Current Contents Connect (CCC)
- Web of Science Core Collection (WoSCC)
- Science Citation Index Expanded (SCI-EXP)
- SCI-EXP, SSCI i/ili A&HCI
- Scopus
- MEDLINE
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