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| MICE DEFICIENT FOR THE 55KD TUMOR-NECROSIS-FACTOR RECEPTOR ARE RESISTANT TO ENDOTOXIC-SHOCK, YET SUCCUMB TO L-MONOCYTOGENES INFECTION |
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| Author(s): PFEFFER K, MATSUYAMA T, KUNDIG TM, WAKEHAM A, KISHIHARA K, SHAHINIAN A, WIEGMANN K, OHASHI PS, KRONKE M, MAK TW |
| Source: CELL Volume: 73 Issue: 3 Pages: 457-467 Published: MAY 7 1993 |
| Times Cited: 1,218 References: 73 |
| Abstract: The multiple biological activities of tumor necrosis factor (TNF) are mediated by two distinct cell surface receptors of 55 kd (TNFRp55) and 75 kd (TNFRp75). Using gene targeting, we generated a TNFRp55-deficient mouse strain. Cells from TNFRp55-/- mutant mice lack expression of TNFRp55 but display normal numbers of high affinity TNFRp75 molecules. Thymocyte development and lymphocyte populations are unaltered, and clonal deletion of potentially self-reactive T cells is not impaired. However, TNF signaling is largely abolished, as judged by the failure of TNF to induce NF-kappaB in T lymphocytes from TNFRp55-deficient mice. The loss of TNFRp55 function renders mice resistant to lethal dosages of either lipopolysaccharides or S. aureus enterotoxin B. In contrast, TNFRp55-deficient mice are severely impaired to clear L. monocytogenes and readily succumb to infection. Thus, the 55 kd TNFR plays a decisive role in the host's defense against microorganisms and their pathogenic factors. |
| Document Type: Article |
| Language: English |
| Reprint Address: PFEFFER, K (reprint author), AMGEN INST, TORONTO M4X 1K9, ON CANADA |
Addresses:
1. UNIV TORONTO, PRINCESS MARGARET HOSP, ONTARIO CANC INST, DEPT MED BIOPHYS, TORONTO M4X 1K9, ONTARIO CANADA
2. UNIV TORONTO, PRINCESS MARGARET HOSP, ONTARIO CANC INST, DEPT IMMUNOL, TORONTO M4X 1K9, ONTARIO CANADA
3. TECH UNIV MUNICH, INST MED MICROBIOL & HYG, W-8000 MUNICH 80, GERMANY |
| Publisher: CELL PRESS, 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 |
| Subject Category: Biochemistry & Molecular Biology; Cell Biology |
| IDS Number: LA743 |
| ISSN: 0092-8674 |
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