Yamaue H, Tanimura H, Iwahashi M, Tsunoda T, Tani M, Tamai M, Inoue M
Department of Gastroenterological Surgery, Wakayama Medical College, Japan.
Gastroenterol Jpn. 1990 Apr;25(2):193-8. doi: 10.1007/BF02776815.
The etiology of idiopathic portal hypertension (IPH) is unknown, although many studies have suggested that it might be an autoimmune disease. The autologous mixed lymphocyte reaction (AMLR) involves the proliferation of T lymphocytes when co-cultured with autologous non-T cells and may reflect immune control mechanisms in vivo. The AMLRs in the spleen and peripheral blood of three patients with IPH were measured and it was shown that the AMLRs both in the spleen and peripheral blood were significantly suppressed compared to those of normal healthy subjects. By allogeneic MLR, there was a tendency that the disturbance of non-T cells was more intensive than that of T cells. The AMLR of peripheral blood did not improve by splenectomy. Thus, the depressed cause of AMLR in patients with IPH was suggested mainly to disturbance of the antigen-presenting ability of non-T cells, and it was suggested that not only the spleen cells, but systemic immune disturbance caused the impairment of AMLR in IPH.
特发性门静脉高压症(IPH)的病因尚不清楚,尽管许多研究表明它可能是一种自身免疫性疾病。自体混合淋巴细胞反应(AMLR)是指T淋巴细胞与自体非T细胞共培养时的增殖反应,可能反映体内的免疫控制机制。对3例IPH患者的脾脏和外周血中的AMLR进行了检测,结果显示与正常健康受试者相比,脾脏和外周血中的AMLR均受到显著抑制。通过异体混合淋巴细胞反应发现,非T细胞的紊乱趋势比T细胞更为明显。脾切除术后外周血的AMLR并未改善。因此,提示IPH患者AMLR降低的原因主要是非T细胞抗原呈递能力的紊乱,并且提示不仅是脾细胞,全身性免疫紊乱也导致了IPH中AMLR的受损。