Ferguson A, MacDonald T T, McClure J P, Holden R J
Lancet. 1975 Apr 19;1(7912):895-7. doi: 10.1016/s0140-6736(75)91689-x.
In an attempt to demonstrate local cell-mediated immunity (C.M.I.) to gliadin in patients with coeliac disease, fragments of jejunal-biopsy specimens were cultured in the presence and absence of alpha-gliadin and the culture-medium was assayed for its capacity to inhibit migration of normal human peripheral-blood leucocytes (i.e., for a migration-inhibition factor [M.I.F.]). No M.I.F. activity was detected in the culture-medium when biopsy specimens from patients with coeliac disease or controls were cultured without added antigen. However, an M.I.F. was secreted into the culture-medium when biopsy specimens from patients with coeliac disease were cultured with alpha-gliadin. These findings suggest that there is a population of lymphocytes which are sensitised to gliadin in the intestinal mucosa of patients with untreated coeliac disease. They support the theory that a local C.M.I. reaction to gliadin may be the cause of villous atrophy and crypt hyperplasia in coeliac disease.
为了证明乳糜泻患者对麦醇溶蛋白存在局部细胞介导免疫（C.M.I.），在有和没有α-麦醇溶蛋白存在的情况下培养空肠活检标本片段，并检测培养基抑制正常人外周血白细胞迁移的能力（即检测迁移抑制因子[M.I.F.]）。当来自乳糜泻患者或对照组的活检标本在不添加抗原的情况下培养时，培养基中未检测到M.I.F.活性。然而，当来自乳糜泻患者的活检标本与α-麦醇溶蛋白一起培养时，有M.I.F.分泌到培养基中。这些发现表明，在未经治疗的乳糜泻患者的肠黏膜中，存在一群对麦醇溶蛋白敏感的淋巴细胞。它们支持这样一种理论，即对麦醇溶蛋白的局部C.M.I.反应可能是乳糜泻中绒毛萎缩和隐窝增生的原因。
