The T-cell receptor and cytotoxicity An anti=idiotype antiserum that inhibits a graft-versus-host reaction does not inhibit cell-mediated cytotoxicity.

An anti-idiotype serum was prepared by injecting BALB anti-AKR serum into (BALB × AKR) F₁ (F1) mice. This serum gave a precipitation band against a hyperimmune BALB anti-AKR serum and inhibited a BALB anti-AKR serum plus complement (C)-mediated cytotoxic reaction. When BALB spleen cells were treated with this serum plus C, their local graft-versus-host reaction against F1 mice was specifically inhibited, proving that T-cell receptors have V regions similar to those of immunoglobulins. On the contrary, the same anti-idiotype serum could not inhibit a cell-mediated Cytotoxicity (CMC) reaction of the same specificity. This would indicate that CMC may be mediated by a population of T-cells which do not necessarily recognize the H-2 antigens through the V region of their receptors.     

The cytokine synthesis by heterozygous carriers of the Toll-like receptor 4 Asp299Gly polymorphism does not differ from that of wild type homozygotes

Previous studies have found that heterozygosity for the A896G mutation of the endotoxin receptor TLR4 confers susceptibility to Gram-negative infections and septic shock. To evaluate the underlying mechanisms, we studied the association of the TLR4 polymorphism with endotoxin-induced cytokine synthesis in human whole blood. Monocyte CD14 density and monocyte count were also determined. Healthy individuals were genotyped by means of a real-time polymerase chain reaction. Plasma concentrations of TNF-alpha, IL-6, and IL-8 were measured by chemiluminescence. No significant differences in cytokine synthesis were observed between heterozygous individuals and homozygous carriers of the wild type allele. Our study suggests that heterozygosity for this TLR4 mutation is not a major factor determining the cytokine response to endotoxin.