Fung J, Köhler H
J Immunol. 1980 Dec;125(6):2489-95.
The cellular mechanism in neonatally suppressed BALB/c mice, which maintains the chronic suppressed state of the TEPC-15 idiotype in the antibody response to phosphorylcholine (PC), was investigated. Cells taken from these suppressed mice cannot transfer suppression to adult BALB/c or affect the in vitro response to PC of adult BALB/c spleen cells. However, spleen cells or T cells from neonatally suppressed mice given to neonatal animals induce chronic suppression of the TEPC-15 idiotype in the anti-PC response. Co-transfer of T cells from neonatally suppressed cells with normal T cells prevented the induction of suppression in neonates. Transfer of T cells from normal or keyhole limpet hemocyanin-primed BALB/c increased the expression of TEPC-15 idiotype in chronically suppressed mice, whereas T cells from neonatally suppressed were ineffective. These findings show that T cells in neonatally suppressed mice can affect the development of immature but not mature cells. The restoration of TEPC-15 expression in neonatally suppressed animals by normal T cells and the failure to induce suppression in neonates by co-transfers of T cells from normal and chronically suppressed mice demonstrate the profound role of an altered T cell compartment in sustaining chronic idiotype suppression.
对新生期受抑制的BALB/c小鼠中维持对磷酸胆碱（PC）抗体反应中TEPC-15独特型慢性抑制状态的细胞机制进行了研究。取自这些受抑制小鼠的细胞不能将抑制作用传递给成年BALB/c小鼠，也不会影响成年BALB/c脾细胞对PC的体外反应。然而，将新生期受抑制小鼠的脾细胞或T细胞给予新生动物，可诱导抗PC反应中TEPC-15独特型的慢性抑制。将新生期受抑制细胞的T细胞与正常T细胞共同转移可防止新生动物诱导抑制。从正常或钥孔戚血蓝蛋白致敏的BALB/c小鼠转移T细胞可增加慢性受抑制小鼠中TEPC-15独特型的表达，而新生期受抑制小鼠的T细胞则无效。这些发现表明，新生期受抑制小鼠中的T细胞可影响未成熟而非成熟细胞的发育。正常T细胞使新生期受抑制动物中TEPC-15表达恢复，以及正常和慢性受抑制小鼠的T细胞共同转移未能在新生动物中诱导抑制，证明了改变的T细胞区室在维持慢性独特型抑制中的重要作用。
