Grissmer S, Cahalan M D, Chandy K G
Department of Physiology and Biophysics, University of California, Irvine 92717.
J Immunol. 1988 Aug 15;141(4):1137-42.
Using the patch clamp whole-cell recording technique, we studied expression of K+ channels in mAb-defined T cell subsets from diseased C3H-lpr/lpr and C3H-gld/gld mice and from healthy C3H-HeJ congenic controls. Both mutant mouse strains develop a lupus-like syndrome accompanied by hyperplasia of a functionally and phenotypically abnormal T cell subset. These defective cells, which are Thy-1.2+ CD4- CD8- B220+ F23.1+, display an abundance of type l K+ channels. Phenotypically similar lymph node T cells from normal C3H-HeJ mice, or young C3H-lpr/lpr mice before the onset of disease, do not display large numbers of type l K+ channels. CD4+ CD8- T cells (helper/inducer) from the mutant mice express a small number of type n K+ channels, and CD4- CD8+ T cells (suppressor/cytotoxic) show a low level of type l or n' K+ channels, as do their phenotypically equivalent counterparts in the normal mouse thymus. These results suggest that the abundant expression of type l K+ channels is a marker for the defective lpr and gld T cell subset and may reflect the "abnormal" proliferative status of these cells.
运用膜片钳全细胞记录技术，我们研究了来自患病的C3H-lpr/lpr和C3H-gld/gld小鼠以及健康的C3H-HeJ同基因对照小鼠中，单克隆抗体定义的T细胞亚群中钾通道的表达情况。两种突变小鼠品系均会发展出类似狼疮的综合征，并伴有功能和表型异常的T细胞亚群增生。这些缺陷细胞为Thy-1.2+ CD4- CD8- B220+ F23.1+，表现出大量的I型钾通道。来自正常C3H-HeJ小鼠或疾病发作前的年轻C3H-lpr/lpr小鼠的表型相似的淋巴结T细胞，并未表现出大量的I型钾通道。突变小鼠的CD4+ CD8- T细胞（辅助/诱导性）表达少量的II型钾通道，而CD4- CD8+ T细胞（抑制/细胞毒性）则表现出低水平的I型或II'型钾通道，正常小鼠胸腺中表型相同的对应细胞也是如此。这些结果表明，I型钾通道的大量表达是缺陷性lpr和gld T细胞亚群的一个标志，可能反映了这些细胞的“异常”增殖状态。
