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Immunophenotypic analysis of b cells in PNH: insights into the generation of circulating naive and memory b cells

bLOOD 2000年第10期96卷 3522-3528页

作者： Richards, SJ Morgan, GJ Hillmen, P Leeds Gen Infirm Haematol Malignancy Diagnost Serv Leeds LS1 3EX W Yorkshire England

Peripheral blood b cells in patients with paroxysmal nocturnal hemoglobinuria (PNH) comprise variable mixtures of normal b cells produced before the onset of disease and glycosylphosphatidylinositol (GPI)-deficient b cells derived from the PNH hematopoietic stem cell. In a detailed phenotypic analysis of 29 patients with PNH, this study shows consistent phenotypic differences between PNH b cells and residual normal b cells. In the majority of patients with active disease, PNH b cells comprised mainly naive cells with a CD27(-)IgM(+)IgD(strong+)IgG(-) phenotype. The proportion of CD27(+) memory cells within this compartment was related to disease duration (Spearman [r(s)] 0.403;P = .030), In PNH patients with predominantly GPI-deficient hematopoiesis, that is, a large granulocyte PNH clone, the residual normal b cells had a predominantly memory (CD27(+)) phenotype. Furthermore, the majority of these memory b cells were not immunoglobulin tig) class switched and had an IgM(+)IgD(+)IgG(-) phenotype. Using PNH as a novel model with which to study b lymphopoiesis, this study provides direct evidence that production of new naive b cells occurs throughout life and that the major population of long-lived memory b cells are IgM(+)IgD(+). Moreover, studies of GPI(-) b cells in 2 patients in remission from PNH suggest that the life span of a b-cell clone can be more than 24 years. (C) 2000 by The American Society of Hematology.

关键词：年龄因素抗原 CD/血液抗原 CD/免疫学抗原 CD27/血液抗原 CD27/免疫学 b淋巴细胞亚群/免疫学 b淋巴细胞亚群/代谢 b淋巴细胞/化学 b淋巴细胞/免疫学 b淋巴细胞/病理学细胞计数克隆细胞/化学克隆细胞/免疫学克隆细胞/病理学糖基磷脂酰肌醇类/缺乏粒细胞/病理学血红蛋白尿阵发性/血液血红蛋白尿阵发性/免疫学血红蛋白尿阵发性/病理学免疫球蛋白G/生物合成免疫球蛋白M/生物合成免疫表型分型青少年成年人老年人女(雌)性人类男(雄)性中年人

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Immunostimulatory CpG-oligonucleotides cause proliferation, cytokine production, and an immunogenic phenotype in chronic lymphocytic leukemia b cells

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bLOOD 2000年第3期95卷 999-1006页

作者： Decker, T Schneller, F Sparwasser, T Tretter, T Lipford, Gb Wagner, H Peschel, C Tech Univ Munich Dept Med 3 D-81675 Munich Germany Tech Univ Munich Inst Med Microbiol & Hyg D-81675 Munich Germany

bacterial DNA and synthetic CpG-oligodeoxynucleotides (ODNs) derived thereof have attracted attention because they activate cells of the immune system in a sequence-dependent manner. Here we investigated the potential of CpG-ODNs to cause proliferation, cytokine production, and regulation of surface molecules in human b-chronic lymphocytic leukemia (CLL) cells, CpG-ODN induced proliferation in both b-CLL cells and normal b cells;however, only b-CLL cells increased proliferative responses when CpG-ODN was added to co-cultures of CD40-ligand transfected mouse fibro blasts (CD40LF) and b cells, Production of interleukin-6 and tumor necrosis factor a was detectable at borderline levels, using CpG-ODN as the only stimulus, In contrast, when CpG-ODN was added to co-cultures of b cells and CD40LF, a strong increase in cytokine production occurred in b-CLL cells as well as in normal b cells, The surface molecules CD40, CD58, CD80, CD86, CD54, and MHC class I molecules were up-regulated in b-CLL cells, whereas CD95 expression was not influenced by CpG-ODN stimulation, The same pattern of surface molecule regulation was observed in normal b cells, but up-regulation of CD40 was significantly stronger in b-CLL cells, Costimulation with CpG-ODN and CD40LF resulted in further up-regulation of CD58, CD80, CD86, and MHC class I molecules, In contrast, CD95 expression induced by CD40-ligation was inhibited by CpG-ODN. CpG-ODN activated b-CLL cells acquired a strong stimulatory capacity toward T cells in allogeneic mixed lymphocyte reaction, This effect was completely inhibited by a combination of anti-CD80 and anti-CD86 monoclonal antibody. Taken together, these findings suggest the possible use of CpG-ODN for immunotherapeutic strategies in patients with b-CLL. (C) 2000 by The American Society of Hematology.

关键词：佐剂免疫/药理学抗原 CD/生物合成抗原 CD/遗传学抗原 CD/免疫学抗原 CD40/免疫学抗原 CD80/免疫学抗原 CD86 抗原肿瘤/生物合成抗原肿瘤/遗传学 b淋巴细胞亚群/细胞学 b淋巴细胞亚群/药物作用 b淋巴细胞亚群/代谢 CD40配体细胞分裂/药物作用共同培养技术细胞因子类/生物合成细胞因子类/遗传学成纤维细胞基因表达调控白血病/药物作用基因 MHCⅠ类组织相容性抗原Ⅰ类/生物合成免疫表型分型白细胞介素6/生物合成白细胞介素6/遗传学淋巴细胞协同作用淋巴细胞培养试验混合膜糖蛋白类/遗传学膜糖蛋白类/免疫学寡脱氧核糖核苷酸类/药理学转染肿瘤细胞培养的肿瘤坏死因子α/生物合成肿瘤坏死因子α/遗传学动物人类小鼠

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Immature b cells in bone marrow express Fas/FasL

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SCANDINAVIAN JOURNAL OF IMMUNOLOGY 2000年第3期51卷 279-284页

作者： Nilsson, N Ingvarsson, S borrebaeck, CAK Univ Lund Dept Immunotechnol S-22007 Lund Sweden

Negative selection is a process by which autoreactive lymphocytes are eliminated from the developing antigen receptor repertoire. The mechanisms regulating negative selection of immature b lymphocytes in the bone marrow are poorly elucidated. Human bone marrow cells were examined in order to investigate the presence of the members of the Fas (APO-1/CD95) system. Here we demonstrate the expression of Fas in immature b lymphocytes (CD10/CD19(+)/CD40(+)/sIg(+)), and the presence of Fas natural ligand (FasL) in CD19(+) bone marrow cells. The observed expression of apoptosis-related molecules might indicate how negative selection of autoreactive b cells can occur in human bone marrow.

关键词：抗原 CD19/生物合成细胞凋亡/免疫学 b淋巴细胞亚群/细胞学 b淋巴细胞亚群/免疫学 b淋巴细胞亚群/代谢 b淋巴细胞亚群/病理学骨髓细胞/细胞学骨髓细胞/免疫学骨髓细胞/代谢骨髓细胞/病理学细胞分化/免疫学细胞系转化 Fas配体蛋白质配体膜糖蛋白类/生物合成前体b细胞淋巴母细胞白血病淋巴瘤/免疫学前体b细胞淋巴母细胞白血病淋巴瘤/代谢受体抗原 b细胞/生物合成肿瘤细胞培养的增量调节/免疫学人类

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Coordinate regulation of b cell differentiation by the transcription factors EbF and E2A

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IMMUNITY 1999年第1期11卷 21-31页

作者： O'Riordan, M Grosschedl, R Univ Calif San Francisco Dept Microbiol & Immunol Howard Hughes Med Inst San Francisco CA 94143 USA

The transcription factors EbF and E2A are required at a similar step in early b cell differentiation. EbF and E2A synergistically upregulate transcription of endogenous b cell-specific genes in a non-b cell line. Here, we examine a genetic collaboration between these factors in regulating b lymphopoiesis. We find that Ebf(+/-)E2a(+/-) mice display a marked defect in pro-b cell differentiation at a stage later than observed in the single homozygous mutant mice. Pro-b cells from Ebf(+/-)E2a(+/-) mice show reduced expression of lymphoid-specific transcripts, including Pax5, Rag1, Rag2, and mb-1. We also show that EbF directly binds and activates the Pax5 promoter. Together, these data show collaboration between EbF and E2A and provide insight into the hierarchy of transcription factors that regulate b lymphocyte differentiation.

关键词：动物新生 b细胞特异性活化蛋白质 b淋巴细胞亚群/代谢 b淋巴细胞亚群/病理学 b淋巴细胞/细胞学 b淋巴细胞/代谢 b淋巴细胞/病理学骨髓细胞/病理学细胞分化/遗传学细胞分化/免疫学 DNA结合蛋白质类/生物合成 DNA结合蛋白质类/遗传学 DNA结合蛋白质类/代谢 DNA结合蛋白质类/生理学增强子元件(遗传学)/免疫学表位 b淋巴细胞/遗传学表位 b淋巴细胞/代谢基因表达调控/免疫学螺旋-环-螺旋构型/遗传学螺旋-环-螺旋构型/免疫学杂合子检测免疫球蛋白λ链/遗传学淋巴细胞减少/遗传学淋巴细胞减少/免疫学淋巴细胞减少/病理学小鼠近交C57bL 小鼠基因敲除分子序列数据核蛋白质类/遗传学核蛋白质类/代谢启动区(遗传学)/免疫学干细胞/代谢干细胞/病理学 TCF转录因子类反式激活因子类/生物合成反式激活因子类/遗传学反式激活因子类/代谢反式激活因子类/生理学转录因子/生物合成转录因子/遗传学转录因子/免疫学转录因子/代谢动物小鼠

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TGF-β receptor controls b cell responsiveness and induction of IgA in vivo

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IMMUNITY 2000年第4期13卷 443-451页

作者： Cazac, bb Roes, J UCL Windeyer Inst Med Sci Dept Med London W1P 6DB England

To determine the role of the pleiotropic cytokine TGF-beta in b cells, we generated mice lacking the TGF-beta receptor (TPR) type II selectively in this cell type through conditional mutagenesis (Cre/loxP). The absence of T beta RII in b cells leads to a reduced life span of conventional b cells, expansion of peritoneal b-1 cells, b cell hyperplasia in Peyer's patches, elevated serum immunoglobulin, and substantial IgG3 responses to a normally weak immunogen. This b cell hyperresponsiveness is associated with a virtually complete serum IgA deficiency. The data reveal differential roles of TPR in homeostasis and antigen responsiveness of a cell subpopulations and establish a critical function of the TGF-beta receptor ligand pair in the induction of IgA responses in vivo.

关键词：抗原/投药和剂量 b淋巴细胞亚群/免疫学 b淋巴细胞亚群/代谢 b淋巴细胞亚群/病理学 b淋巴细胞/免疫学 b淋巴细胞/代谢细胞分裂/遗传学细胞分裂/免疫学鸡交叉遗传聚蔗糖/投药和剂量聚蔗糖/免疫学 IgA缺乏/遗传学 IgA缺乏/免疫学 IgA缺乏/病理学免疫球蛋白A/生物合成免疫球蛋白同型/生物合成肠黏膜/免疫学肠黏膜/代谢肠黏膜/病理学淋巴细胞活化/遗传学小鼠近交bALbC 小鼠基因敲除硝基酚类/投药和剂量硝基酚类/免疫学淋巴集结/免疫学淋巴集结/代谢淋巴集结/病理学苯乙酸酯类蛋白质丝氨酸苏氨酸激酶受体转化生长因子β/缺乏受体转化生长因子β/遗传学受体转化生长因子β/生理学序列缺失丙种球蛋白类/投药和剂量丙种球蛋白类/免疫学动物女(雌)性小鼠

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