Distinct Roles of Lymphotoxin α and the Type I Tumor Necrosis Factor (TNF) Receptor in the Establishment of Follicular Dendritic Cells from Non–Bone Marrow–derived Cells
| Autor: | Jinho Kim, Guangming Huang, Dori A. Thomas, Hector Molina, Moon H. Nahm, Yang Xin Fu, David D. Chaplin, Mitsuru Matsumoto |
|---|---|
| Rok vydání: | 1997 |
| Předmět: |
Lymphotoxin alpha
medicine.drug_class Complement receptor 1 Immunology Bone Marrow Cells Mice Transgenic Spleen Biology Monoclonal antibody Article Receptors Tumor Necrosis Factor Immunoenzyme Techniques Mice medicine Animals Immunology and Allergy Lymphotoxin-alpha Bone Marrow Transplantation Mice Knockout Follicular dendritic cells Germinal center Dendritic Cells Germinal Center Molecular biology medicine.anatomical_structure Tumor necrosis factor alpha Bone marrow biology.gene |
| Zdroj: | The Journal of Experimental Medicine |
| ISSN: | 1540-9538 0022-1007 |
| DOI: | 10.1084/jem.186.12.1997 |
| Popis: | In mice deficient in either lymphotoxin alpha (LT-alpha) or type I tumor necrosis factor receptor (TNFR-I), organized clusters of follicular dendritic cells (FDC) and germinal centers (GC) are absent from the spleen. We investigated the role of LT-alpha and TNFR-I in the establishment of spleen FDC and GC structure by using reciprocal bone marrow (BM) transfer. When LT-alpha-deficient mice were reconstituted with wild-type BM, FDC organization and the ability to form GC were restored, indicating that the LT-alpha-expressing cells required to establish organized FDC are derived from BM. The role of LT-alpha in establishing organized FDC structure was further investigated by the transfer of complement receptor 1 and 2 (CR1/2)-deficient BM cells into LT-alpha-deficient mice. Organized FDC were identified with both the FDC-M1 and anti-CR1 monoclonal antibodies in these BM-chimeric mice, indicating that these cells were derived from the LT-alpha-deficient recipient. Thus, expression of LT-alpha in the BM-derived cells, but not in the non-BM-derived cells, is required for the maturation of FDC from non-BM precursor cells. In contrast, when TNFR-I-deficient mice were reconstituted with wild-type BM, they showed no detectable FDC clusters or GC formation. This indicates that TNFR-I expression on non-BM-derived cellular components is necessary for the establishment of these lymphoid structures. TNFR-I-deficient BM was able to restore FDC organization and GC formation in LT-alpha-deficient mice, indicating that formation of these structures does not require TNFR-I expression on BM-derived cells. The data in this study demonstrate that FDC organization and GC formation are controlled by both LT-alpha-expressing BM-derived cells and by TNFR-I-expressing non-BM-derived cells. |
| Databáze: | OpenAIRE |
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