Mice deficient for the 55 kd tumor necrosis factor receptor are resistant to endotoxic shock, yet succumb to L. monocytogenes infection.

摘要: Abstract The multiple biological activities of tumor necrosis factor (TNF) are mediated by two distinct cell surface receptors 55 kd (TNFRp55) and 75 (TNFRp75). Using gene targeting, we generated a TNFRp55-deficient mouse strain. Cells from TNFRp55-/- mutant mice lack expression TNFRp55 but display normal numbers high affinity TNFRp75 molecules. Thymocyte development lymphocyte populations unaltered, clonal deletion potentially self-reactive T cells is not impaired. However, TNF signaling largely abolished, as judged the failure to induce NF-κB in lymphocytes loss function renders resistant lethal dosages either lipopolysaccharides or S. aureus enterotoxin B. In contrast, severely impaired clear L. monocytogenes readily succumb infection. Thus, TNFR plays decisive role host's defense against microorganisms their pathogenic factors.