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Publication : Lymphotoxin-β receptor signaling through NF-κB2-RelB pathway reprograms adipocyte precursors as lymph node stromal cells.

First Author  Bénézech C Year  2012
Journal  Immunity Volume  37
Issue  4 Pages  721-34
PubMed ID  22940098 Mgi Jnum  J:188330
Mgi Id  MGI:5440341 Doi  10.1016/j.immuni.2012.06.010
Citation  Benezech C, et al. (2012) Lymphotoxin-beta Receptor Signaling through NF-kappaB2-RelB Pathway Reprograms Adipocyte Precursors as Lymph Node Stromal Cells. Immunity 37(4):721-34
abstractText  Lymph node development during embryogenesis involves lymphotoxin-beta receptor engagement and subsequent differentiation of a poorly defined population of mesenchymal cells into lymphoid tissue organizer cells. Here, we showed that embryonic mesenchymal cells with characteristics of adipocyte precursors present in the microenvironment of lymph nodes gave rise to lymph node organizer cells. Signaling through the lymphotoxin-beta receptor controlled the fate of adipocyte precursor cells by blocking adipogenesis and instead promoting lymphoid tissue stromal cell differentiation. This effect involved activation of the NF-kappaB2-RelB signaling pathway and inhibition of the expression of the key adipogenic factors Ppargamma and Cebpalpha. In vivo organogenesis assays show that embryonic and adult adipocyte precursor cells can migrate into newborn lymph nodes and differentiate into a variety of lymph node stromal cells. Thus, we propose that adipose tissues act as a source of lymphoid stroma for lymph nodes and other lymphoid structures associated with fat.
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