Bunjes D, Wiesneth M, Hertenstein B, Schmeiser T, Arnold R, Heit W
Department of Internal Medicine, Ulm University Hospital, FRG.
Bone Marrow Transplant. 1990 Nov;6(5):309-14.
We have investigated the clinical and immunological features of 10 cases of graft failure after T cell-depleted marrow transplantation. In addition, the hypothesis that the process of graft failure can be reversed by immunosuppressive therapy with cyclosporin + steroids +/- monoclonal antibodies was tested in seven patients. Early graft failures (before day 50) presented a uniform clinical syndrome with a host T lymphocytosis preceding the loss of the graft. In the majority of cases of late graft failure (after day 50) a syndrome comprising delayed granulopoietic regeneration, fever of unknown origin and abdominal symptoms was observed. Surface marker analysis of peripheral blood and bone marrow lymphocytes implicated a population of CD3+, CD8+, DR+ host T lymphocytes with a frequent co-expression of the Leu7+ antigen in the pathogenesis of graft failure. Immunosuppressive therapy reversed graft failure in the three cases of incomplete graft failure (i.e. with residual reticulocytes) and failed in the four cases of complete graft failure (i.e. no residual reticulocytes).
我们研究了10例T细胞去除的骨髓移植后移植物衰竭的临床和免疫学特征。此外,还对7例患者进行了环孢素+类固醇+/-单克隆抗体免疫抑制治疗能否逆转移植物衰竭过程的假设进行了测试。早期移植物衰竭(移植后50天之前)表现出一种统一的临床综合征,在移植物丢失之前出现宿主T淋巴细胞增多。在大多数晚期移植物衰竭(移植后50天之后)病例中,观察到一种包括延迟粒细胞生成再生、不明原因发热和腹部症状的综合征。外周血和骨髓淋巴细胞的表面标志物分析表明,在移植物衰竭的发病机制中,一群CD3 +、CD8 +、DR +宿主T淋巴细胞经常共同表达Leu7 +抗原。免疫抑制治疗在3例不完全移植物衰竭(即有残余网织红细胞)病例中逆转了移植物衰竭,而在4例完全移植物衰竭(即无残余网织红细胞)病例中失败。