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丝裂原诱导的慢性B淋巴细胞白血病和免疫细胞瘤细胞群体中免疫球蛋白重链类别分泌的转换

Mitogen-induced switching of immunoglobulin heavy-chain class secretion in chronic B-lymphocytic leukaemia and immunocytoma cell populations.

作者信息

Juliusson G, Robèrt K H, Hammarström L, Smith C I, Biberfeld G, Gahrton G

出版信息

Scand J Immunol. 1983 Jan;17(1):51-9. doi: 10.1111/j.1365-3083.1983.tb00765.x.

Abstract

Lymphocytes from peripheral blood, bone marrow, and lymph nodes from six patients with chronic B-lymphoproliferative disease were studied. Two of the patients had a polymorphic immunocytoma with surface membrane immunoglobulin phenotype mu kappa. Four patients had chronic B-lymphocytic leukaemia (CLL) with the phenotypes mu kappa, mu delta kappa, mu lambda, and mu delta lambda, respectively. In no case did the monoclonal cell populations express gamma chains on the surface, and none produced monoclonal immunoglobulin in vivo. The malignant B lymphocytes were cultured in the presence of polyclonal B-cell activators. Immunoglobulin secretion was detected with the protein A plaque assay and with a modification of the reversed haemolysis-in-agar plaque assay. Immunoglobulin secretion was induced in four of the cell populations. In both the immunocytomas and in one of the CLL cell clones the heat-inactivated Staphylococcus aureus strain Cowan I induced secretion of IgG, as well as IgM, associated only with the same light chain as was expressed on the surface of the unstimulated cells. Thus, mitogens can induce immunoglobulin secretion in vitro in malignant B lymphocytes, and Cowan I bacteria also have the ability to induce a switch of immunoglobulin production from IgM to IgG in a fraction of the leukaemic cell populations.

摘要

对6例慢性B淋巴细胞增殖性疾病患者外周血、骨髓和淋巴结中的淋巴细胞进行了研究。其中2例患者患有具有表面膜免疫球蛋白表型μκ的多形性免疫细胞瘤。4例患者患有慢性B淋巴细胞白血病(CLL),其表型分别为μκ、μδκ、μλ和μδλ。在任何情况下,单克隆细胞群体在表面均不表达γ链,且无一例在体内产生单克隆免疫球蛋白。将恶性B淋巴细胞在多克隆B细胞激活剂存在的情况下进行培养。用蛋白A空斑试验和改良的琼脂反向溶血空斑试验检测免疫球蛋白分泌。在4个细胞群体中诱导了免疫球蛋白分泌。在免疫细胞瘤和其中一个CLL细胞克隆中,热灭活的金黄色葡萄球菌考恩I株诱导了IgG以及IgM的分泌,且仅与未刺激细胞表面表达的相同轻链相关。因此,丝裂原可在体外诱导恶性B淋巴细胞分泌免疫球蛋白,考恩I细菌也有能力在一部分白血病细胞群体中诱导免疫球蛋白产生从IgM向IgG的转换。

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