Tanaka T, Nagasaka Y, Kitamura F, Kuida K, Suwa H, Miyasaka M
Department of Immunology, Tokyo Metropolitan Institute of Medical Science, Japan.
Eur J Immunol. 1993 Jun;23(6):1378-80. doi: 10.1002/eji.1830230629.
Autoimmune MRL/MP-lpr/lpr (MRL/lpr) mice spontaneously develop a systemic lupus erythematosus-like disease accompanied by a profound lymphadenopathy that consists of CD4-8-B220+ alpha beta T cells. By the use of cross-linking experiments with radiolabeled interleukin-2 (IL-2), these abnormal T cells have been reported to constitutively express the IL-2 receptor beta chain (IL-2R beta), a signal transducing component of IL-2R, in the absence of the alpha chain (IL-2R alpha). To critically reevaluate the role of the IL-2/IL-2R pathway in the pathogenesis of lymphadenopathy we examined expression of the IL-2R alpha and IL-2R beta in MRL/lpr mice by 125I-IL-2 binding analysis and also by flow cytometric analysis using monoclonal antibodies against each component of the receptor. We found that, contrary to the previous report, the CD4-8-B220+ alpha beta T cells in lymph node (LN) of MRL/lpr mice were negative for both IL-2R alpha and IL-2R beta expression. The lpr liver CD4-8-B220+ alpha beta T cells that had been implicated in the genesis of these abnormal LN T cells were also negative for IL-2R beta expression. Therefore, our results indicate that the IL-2/IL-2R system plays little role, if any, in the expansion of abnormal CD4-8-B220+ alpha beta T cells in MRL/lpr mice.
自身免疫性MRL/MP-lpr/lpr（MRL/lpr）小鼠会自发发展出一种系统性红斑狼疮样疾病，并伴有严重的淋巴结病，该淋巴结病由CD4 - 8 - B220 + αβ T细胞组成。通过使用放射性标记的白细胞介素-2（IL-2）进行交联实验，据报道这些异常T细胞在缺乏α链（IL-2Rα）的情况下组成性表达IL-2受体β链（IL-2Rβ），IL-2Rβ是IL-2R的信号转导成分。为了严格重新评估IL-2/IL-2R途径在淋巴结病发病机制中的作用，我们通过125I-IL-2结合分析以及使用针对受体各成分的单克隆抗体进行流式细胞术分析，检测了MRL/lpr小鼠中IL-2Rα和IL-2Rβ的表达。我们发现，与之前的报道相反，MRL/lpr小鼠淋巴结（LN）中的CD4 - 8 - B220 + αβ T细胞在IL-2Rα和IL-2Rβ表达上均为阴性。曾被认为与这些异常LN T细胞起源有关的lpr肝脏CD4 - 8 - B220 + αβ T细胞在IL-2Rβ表达上也为阴性。因此，我们的结果表明，IL-2/IL-2R系统在MRL/lpr小鼠异常CD4 - 8 - B220 + αβ T细胞的扩增中几乎不起作用（如果有作用的话）。
