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淋巴瘤和白血病中脾脏粒细胞生成及集落刺激活性的产生

Splenic granulocytopoiesis and production of colony-stimulating activity in lymphoma and leukemia.

作者信息

Greenberg P L, Steed S M

出版信息

Blood. 1981 Jan;57(1):119-29.

PMID:6969608
Abstract

Spleen cell production of granulocyte-macrophage colony stimulating activity (CSA) and colony forming capacity (CFU-GM) from 59 patients with Hodgkin's and non-Hodgkin's lymphoma, acute (AML) and chronic myeloid leukemia (CML), and control subjects was quantified to evaluate local cellular potential for modulating splenic granulocytopoiesis. Mononuclear spleen cell conditioned media stimulated myeloid CFU-GM by human nonadherent marrow target cells. In contrast to conditioned media produced by marrow and peripheral blood cells, the vast majority of spleen CSA was generated by nonadherent lymphoid cells rather than adherent monocytic cells. The nonadherent cells producing CSA were non-T cells (assessed by sheep erythrocyte rosetting), with 98% +/- 2% CSA produced by the nonrosetted fraction (B lymphocytes and null cells), and had a peak density heavier than that of the adherent spleen CSA-producing cells. Dose response curves demonstrated significantly increased cellular CSA production from patients with lymphomas and AML in remission. In a high proportion of patients, foci of immature granulocytic cells were found by specific cytochemical staining of histologic sections of spleens. A limited degree of splenic granulocytopoiesis was demonstrated morphologically and by CFU-GM incidence. CSA was not detectable in conditioned medium prepared from nonadherent spleen cells from 5 patients with CML, due to a nondialyzable substances(s) produced by the nonadherent cells which inhibited normal CFU-GM response to CSA. The high CFU-GM incidence and extensive leukemic granulocytopoiesis present in the CML spleens suggests diminished effect of this inhibitor on leukemic as opposed to normal granulocytic precursor cell proliferation.

摘要

对59例霍奇金淋巴瘤和非霍奇金淋巴瘤、急性髓系白血病(AML)和慢性髓系白血病(CML)患者以及对照受试者的脾细胞产生粒细胞 - 巨噬细胞集落刺激活性(CSA)和集落形成能力(CFU - GM)进行定量,以评估局部细胞调节脾粒细胞生成的潜力。单核脾细胞条件培养基可刺激人非贴壁骨髓靶细胞形成髓系CFU - GM。与骨髓和外周血细胞产生的条件培养基不同,绝大多数脾CSA是由非贴壁淋巴细胞而非贴壁单核细胞产生的。产生CSA的非贴壁细胞是非T细胞(通过绵羊红细胞花环试验评估),98%±2%的CSA由非花环形成部分(B淋巴细胞和裸细胞)产生,其峰值密度比产生CSA的贴壁脾细胞的峰值密度大。剂量反应曲线表明,缓解期淋巴瘤和AML患者的细胞CSA产生显著增加。通过脾脏组织切片的特异性细胞化学染色,在高比例患者中发现了未成熟粒细胞灶。形态学和CFU - GM发生率均显示有一定程度的脾粒细胞生成。5例CML患者的非贴壁脾细胞制备的条件培养基中未检测到CSA,这是由于非贴壁细胞产生的一种不可透析物质抑制了正常CFU - GM对CSA的反应。CML脾脏中高CFU - GM发生率和广泛的白血病粒细胞生成表明,与正常粒细胞前体细胞增殖相比,这种抑制剂对白血病细胞的作用减弱。

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