Baran D, Lantz O, Dosquet P, Sfaksi A, Druet P
Inserm U28-Hôpital Broussais, Paris, France.
Clin Exp Immunol. 1988 Sep;73(3):401-5.
In autoimmune diseases, mitogen-induced IL-2 production in vitro is generally considered to be diminished despite evidence of lymphoid hyperactivity in vivo. HgCl2 is known to cause T-dependent polyclonal B cell activation in Brown-Norway (BN) rats, resulting in autoimmune disease. We show here that the IL-2 producing capacity of cells from HgCl2-treated BN rats is low, but that HgCl2 treatment in vitro (10(-7) M) enhances IL-2 production of normal BN splenocytes. Lewis (LEW) rats are resistant to HgCl2-induced autoimmune disease. HgCl2 treatment of these rats in vivo does not significantly decrease the IL-2 production of their splenocytes. However, HgCl2 treatment of normal LEW splenocytes in vitro enhances their IL-2 production but this requires an HgCl2 concentration ten times greater (10(-6) M) in LEW than in BN rats. These findings are discussed in an attempt to resolve the paradox between the in vivo immune hyperactivity seen in HgCl2-treated BN rats, and the apparently low IL-2 production of their splenocytes in vitro.
在自身免疫性疾病中，尽管体内存在淋巴细胞活性亢进的证据，但体外有丝分裂原诱导的白细胞介素-2（IL-2）产生通常被认为是减少的。已知氯化汞（HgCl2）可导致棕色挪威（BN）大鼠发生T细胞依赖性多克隆B细胞活化，进而引发自身免疫性疾病。我们在此表明，HgCl2处理的BN大鼠细胞产生IL-2的能力较低，但体外HgCl2处理（10^(-7) M）可增强正常BN脾细胞的IL-2产生。刘易斯（LEW）大鼠对HgCl2诱导的自身免疫性疾病具有抗性。体内用HgCl2处理这些大鼠不会显著降低其脾细胞的IL-2产生。然而，体外用HgCl2处理正常LEW脾细胞可增强其IL-2产生，但这需要的HgCl2浓度在LEW大鼠中比在BN大鼠中高十倍（10^(-6) M）。对这些发现进行了讨论，试图解决在HgCl2处理的BN大鼠中观察到的体内免疫亢进与它们的脾细胞在体外明显较低的IL-2产生之间的矛盾。
