Regulation of peripheral lymph node genesis by the tumor necrosis factor family member TRANCE
| Autor: | Régis Josien, Paul D. Rennert, Steffen Jung, Jaerang Rho, Yongwon Choi, Yaneth Castellanos, Reina E. Mebius, John D. MacMicking, Brian Wong, Nacksung Kim, Tom Cupedo, Dong-Ku Kim |
|---|---|
| Rok vydání: | 2000 |
| Předmět: |
medicine.medical_specialty
CD3 Complex medicine.medical_treatment Transgene tumor necrosis factor organogenesis Immunology Cell Population TRANCE Spleen Mice Transgenic Biology Mice Internal medicine lymphotoxin medicine Immunology and Allergy Animals education Lymph node education.field_of_study B-Lymphocytes Membrane Glycoproteins Receptor Activator of Nuclear Factor-kappa B Tumor Necrosis Factor-alpha RANK Ligand lymph node Molecular biology Cytokine medicine.anatomical_structure Lymphotoxin Endocrinology CD4 Antigens Leukocyte Common Antigens Tumor necrosis factor alpha Original Article Lymph Nodes Carrier Proteins |
| Zdroj: | The Journal of Experimental Medicine |
| ISSN: | 0022-1007 |
| Popis: | Proper lymph node (LN) development requires tumor necrosis factor-related activation-induced cytokine (TRANCE) expression. Here we demonstrate that the defective LN development in TRANCE(-/)- mice correlates with a significant reduction in lymphotoxin (LT)alphabeta(+)alpha(4)beta(7)(+)CD45(+)CD4(+)CD3(-) cells and their failure to form clusters in rudimentary mesenteric LNs. Transgenic TRANCE overexpression in TRANCE(-/)- mice results in selective restoration of this cell population into clusters, and results in full LN development. Transgenic TRANCE-mediated restoration of LN development requires LTalphabeta expression on CD45(+) CD4(+)CD3(-) cells, as LNs could not be induced in LTalpha(-/)- mice. LTalpha(-/)- mice also showed defects in the fate of CD45(+)CD4(+)CD3(-) cells similar to TRANCE(-/)- mice. Thus, we propose that both TRANCE and LTalphabeta regulate the colonization and cluster formation by CD45(+) CD4(+)CD3(-) cells in developing LNs, the degree of which appears to correlate with the state of LN organogenesis. |
| Databáze: | OpenAIRE |
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