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免疫球蛋白同种异型合成的主动抑制。3. 鉴定T细胞是脾脏、胸腺、淋巴结和骨髓来源细胞抑制作用的原因。

Active suppression of immunoglobulin allotype synthesis. 3. Identification of T cells as responsible for suppression by cells from spleen, thymus, lymph node, and bone marrow.

作者信息

Herzenberg L A, Chan E L, Ravitch M M, Riblet R J, Herzenberg L A

出版信息

J Exp Med. 1973 Jun 1;137(6):1311-24. doi: 10.1084/jem.137.6.1311.

Abstract

Thymus-derived cells (T cells) that actively suppress production of IgG2a immunoglobulins carrying the Ig-1b allotype have been found in adult (SJL x BALB/c)F(1) mice exposed to anti-Ig-1b early in life. The suppression is specific for Ig-1b. The allelic product, Ig-1a, is unaffected. Spleen, lymph node, bone marrow, or thymus cells from suppressed mice suppress production of Ig-1b by syngeneic spleen cells from normal F(1) mice. When a mixture of suppressed and normal cells is transferred into lethally irradiated BALB/c mice, there is a short burst of Ig-1b production after which Ig-1b levels in the recipient fall rapidly below detectability. Pretreatment of the cells from the suppressed mice with antiserum specific for T cells (anti-Thy-1b) plus complement before mixture destroys the suppressing activity. Similar results with suppressor cells were obtained in vitro using Mishell-Dutton cultures. Mixture of spleen cells from suppressed animals with sheep erythrocyte (SRBC)-primed syngeneic normal spleen before culture suppresses Ig-1b plaque-forming cell (PFC) formation while leaving Ig-1a PFC unaffected. Treatment of the suppressed spleen with anti-Thy-1b before transfer removes the suppressing activity.

摘要

在生命早期接触过抗Ig-1b的成年(SJL×BALB/c)F1小鼠中,发现了能积极抑制携带Ig-1b同种异型的IgG2a免疫球蛋白产生的胸腺来源细胞(T细胞)。这种抑制作用对Ig-1b具有特异性。其等位基因产物Ig-1a不受影响。来自受抑制小鼠的脾脏、淋巴结、骨髓或胸腺细胞可抑制正常F1小鼠同基因脾脏细胞产生Ig-1b。当将受抑制细胞与正常细胞的混合物转移到经致死剂量照射的BALB/c小鼠体内时,会有短暂的Ig-1b产生高峰,之后受体小鼠体内的Ig-1b水平迅速降至检测不到的水平。在混合之前,用抗T细胞特异性抗血清(抗Thy-1b)加补体对受抑制小鼠的细胞进行预处理可破坏抑制活性。在体外使用米舍尔-达顿培养法也得到了与抑制细胞类似的结果。在培养前,将受抑制动物的脾脏细胞与用绵羊红细胞(SRBC)致敏的同基因正常脾脏细胞混合,可抑制Ig-1b空斑形成细胞(PFC)的形成,而Ig-1a PFC不受影响。在转移前用抗Thy-1b处理受抑制的脾脏可消除抑制活性。

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