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Ek分子在响应LDHB产生抑制性T细胞过程中的作用。

Role of the Ek molecule in the generation of suppressor T cells in response to LDHB.

作者信息

Baxevanis C N, Ishii N, Nagy Z A, Klein J

出版信息

Scand J Immunol. 1982 Jul;16(1):25-31. doi: 10.1111/j.1365-3083.1982.tb00695.x.

Abstract

The role of the Ek (E alpha kE beta k) molecule in the generation of suppressor T (Ts) cells specific for lactate dehydrogenase B (LDHB) was studied using different approaches. First, lymph node cells from LDHB-primed B10.A(2R) (AkEk) nonresponder mice were shown to suppress the LDHB-specific and Ak-restricted proliferative response of T cells from the congenic responder strain B10.A(4R), which does not express E molecules (AkEo). Similarly, lymph node cells from primed CBA (AkEk) mice suppressed the anti-LDHB response of Lyt-1+Lyt-2-T cells (depleted of Lyt-2-bearing Ts cells) from the same mice. Second, in vitro priming of 2R (AkEk) T cells with LDHB-pulsed 4R (AkEo) antigen-presenting cells (APC) generated T-cell proliferation but not suppression. Third, nonresponder 2R mice were turned into responders by injecting them with LDHB-pulsed 4R APC or monoclonal Ia.m7 antibody that blocks the Ek molecule. The data demonstrate that expression of Ek molecules by the APC is necessary to generate LDHB-specific Ts cells, which in turn prevent the proliferation of Lyt-1+Lyt-2- (probably helper) cells recognizing the same antigen in the context of the Ak molecule.

摘要

采用不同方法研究了Ek(EαkEβk)分子在产生乳酸脱氢酶B(LDHB)特异性抑制性T细胞(Ts细胞)中的作用。首先,来自用LDHB免疫的B10.A(2R)(AkEk)无反应小鼠的淋巴结细胞,被证明能抑制来自同基因反应性品系B10.A(4R)(不表达E分子,AkEo)的T细胞的LDHB特异性和Ak限制性增殖反应。同样,来自免疫的CBA(AkEk)小鼠的淋巴结细胞抑制了来自同一小鼠的Lyt-1⁺Lyt-2⁻T细胞(去除了带有Lyt-2的Ts细胞)的抗LDHB反应。其次,用LDHB脉冲处理的4R(AkEo)抗原呈递细胞(APC)对2R(AkEk)T细胞进行体外免疫,可产生T细胞增殖,但不产生抑制作用。第三,通过给无反应的2R小鼠注射LDHB脉冲处理的4R APC或阻断Ek分子的单克隆Ia.m7抗体,可使其转变为反应性小鼠。数据表明,APC表达Ek分子对于产生LDHB特异性Ts细胞是必要的,而这些Ts细胞反过来又会阻止在Ak分子背景下识别相同抗原的Lyt-1⁺Lyt-2⁻(可能是辅助性)细胞的增殖。

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