Fischbach M
J Immunol. 1984 Nov;133(5):2365-8.
The effect of the single autosomal recessive gene lpr on antigen presentation was studied. MRL/Mp-lpr/lpr, C3H/HeJ-lpr/lpr, C57BL/6J-lpr/lpr, and their normal congenic partners were investigated. Mice bearing the lpr gene were unable to respond to TNP-KLH when presented by syngeneic antigen-presenting cells. The congenic normal partners gave a brisk response. Mixing experiments demonstrated that the defect resided with the lpr responding T cell and not with the lpr antigen-presenting cell. Antigen-presenting cells from lpr mice were capable of inducing T cell proliferation in normal congenic partners, whereas antigen-presenting cells from normal mice failed to stimulate lpr T cells. This defect was intrinsic to an Lyt-1+2- cell. Pharmacologic restoration was attempted by in vivo and in vitro administration of interleukin 2. However, cells from lpr mice remained unaffected. The relationship of these findings to autoimmunity is discussed.
研究了单个常染色体隐性基因lpr对抗抗原呈递的影响。对MRL/Mp-lpr/lpr、C3H/HeJ-lpr/lpr、C57BL/6J-lpr/lpr及其正常同基因对照进行了研究。携带lpr基因的小鼠在由同基因抗原呈递细胞呈递TNP-KLH时无法产生反应。同基因正常对照则产生快速反应。混合实验表明，缺陷存在于lpr反应性T细胞而非lpr抗原呈递细胞中。来自lpr小鼠的抗原呈递细胞能够在正常同基因对照中诱导T细胞增殖，而来自正常小鼠的抗原呈递细胞则无法刺激lpr T细胞。这种缺陷是Lyt-1+2-细胞所固有的。尝试通过体内和体外给予白细胞介素2进行药理学恢复。然而，来自lpr小鼠的细胞仍然未受影响。讨论了这些发现与自身免疫的关系。
