Levin D M, Lipsky P E, Kirkpatrick C H
Am J Med. 1975 Jan;58(1):129-34. doi: 10.1016/0002-9343(75)90543-4.
A 46 year old man presented with selective hypogammaglobulinemia, malabsorption and long-standing secondary malnutrition. Although the patient had essentially unmeasurable levels of immunoglobulins G (IgG), M (IgA), he had normal levels of immunoglobulin E (IgE). He was found to be anergic when tested for the delayed cutaneous hypersensitivity reaction. Evaluation of his cell-mediated immunity in vivo and in vitro suggested one discrete lesion, a defective production of the lymphocyte mediator macrophage migration inhibitory factor. With improved nutrition the patient "repaired" this defect in the "efferent" limb of cellular immunity and was no longer anergic.
一名46岁男性出现选择性低丙种球蛋白血症、吸收不良和长期继发性营养不良。尽管该患者的免疫球蛋白G(IgG)、M(IgA)水平基本无法测出,但免疫球蛋白E(IgE)水平正常。在进行迟发性皮肤超敏反应检测时,发现他无反应。对其体内和体外细胞介导免疫的评估提示存在一个单一病变,即淋巴细胞介质巨噬细胞移动抑制因子产生缺陷。随着营养状况改善,患者在细胞免疫的“传出”支中“修复”了这一缺陷,不再无反应。