McCormack J E, Kappler J, Marrack P
Howard Hughes Medical Institute, University of Colorado Health Sciences Center, Denver 80206.
Proc Natl Acad Sci U S A. 1994 Mar 15;91(6):2086-90. doi: 10.1073/pnas.91.6.2086.
The T-cell response to pigeon cytochrome c peptide, residues 88-104 (pcytC), in B10.BR mice is mediated largely by cells bearing both V beta 3 and V alpha 11 variable regions of the T-cell antigen receptor. These cells are, therefore, reactive with the superantigen staphylococcal enterotoxin A (SEA). Recent reports have shown that in vivo exposure to superantigen can lead to deletion of superantigen-reactive T cells from the pool of mature T cells in the periphery. Here we show that upon cotreatment of animals with both SEA and pcytC, bulk deletion of the population of SEA-reactive cells is maintained, while the subpopulation of SEA-reactive T cells that also responds to pcytC is not deleted but instead proliferates in response to pcytC. These results are discussed with regard to mechanisms regulating the balance between T-cell tolerance and T-cell activation in vivo.
在B10.BR小鼠中,T细胞对鸽细胞色素c肽(第88 - 104位氨基酸,pcytC)的反应很大程度上由带有T细胞抗原受体Vβ3和Vα11可变区的细胞介导。因此,这些细胞对超抗原葡萄球菌肠毒素A(SEA)具有反应性。最近的报告表明,体内暴露于超抗原可导致外周成熟T细胞池中对超抗原反应性的T细胞缺失。在此我们表明,在用SEA和pcytC共同处理动物后,对SEA反应性细胞群体的大量缺失得以维持,而对SEA反应且也对pcytC有反应的T细胞亚群未被删除,而是对pcytC发生增殖反应。本文就体内调节T细胞耐受性和T细胞活化之间平衡的机制对这些结果进行了讨论。