Smith E M, Meyer W J, Blalock J E
Science. 1982 Dec 24;218(4579):1311-2. doi: 10.1126/science.6183748.
Infection of hypophysectomized mice with Newcastle disease virus caused a time-dependent increase in corticosterone and interferon production. Prior treatment with dexamethasone completely inhibited the virus-induced elevation in corticosterone concentration, but did not significantly alter the interferon response. Lymphocytes appear to be the most likely source of an adrenocorticotropin-like substance that is responsible for the increased corticosterone, since spleen cells from the virus-infected, but not from control or dexamethasone-treated, hypophysectomized mice showed positive immunofluorescence with antibody to adrenocorticotropin-(1-13 amide). Thus the adrenocorticotropin-like material and interferon appear to be coordinately induced the differentially controlled products of different genes. These findings strongly suggest the existence of a lymphoid-adrenal axis.
用新城疫病毒感染垂体切除的小鼠会导致皮质酮和干扰素产量随时间增加。预先用地塞米松处理可完全抑制病毒诱导的皮质酮浓度升高,但对干扰素反应没有显著影响。淋巴细胞似乎是导致皮质酮增加的促肾上腺皮质激素样物质的最可能来源,因为来自病毒感染的垂体切除小鼠而非对照或地塞米松处理的垂体切除小鼠的脾细胞,在用抗促肾上腺皮质激素-(1-13酰胺)抗体检测时呈现阳性免疫荧光。因此,促肾上腺皮质激素样物质和干扰素似乎是由不同基因协调诱导和差异控制的产物。这些发现强烈提示存在淋巴-肾上腺轴。