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Generation of murine dendritic cells from flt3-ligand-supplemented bone marrow cultures

BLOOD 2000年第9期96卷 3029-3039页

作者： Brasel, K De Smedt, T Smith, JL Maliszewski, CR Immunex Res & Dev Corp Dept Immunobiol Seattle WA 98101 USA Immunex Res & Dev Corp Dept Discovery Res Seattle WA 98101 USA

Murine dendritic cells (DCs) can be classified into at least 2 subsets, "myeloid-related" (CD11(bright), CD8 alpha (-)) and "lymphoid-related" (CD11b(dull), CD8 alpha (+)), but the absolute relationship between the 2 remains unclear. Methods of generating DCs from bone marrow (BM) precursors in vitro typically employ granulocyte-macrophage colony-stimulating factor (GM-CSF) as the principal growth factor, and the resultant DCs exhibit a myeloidlike phenotype, Here we describe a flt3-ligand (FL)-dependent BM culture system that generated DCs with more diverse phenotypic characteristics. Murine BM cells cultured at high density in recombinant human FL for 9 days developed into small lymphoid-sized cells, most of which expressed CD11c, CD86, and major histocompatibility complex (MHC) class II. The CD11c(+) population could be divided into 2 populations on the basis of the level of expression of CD11b, which may represent the putative myeloid- and lymphoid-related subsets. The FL in vitro-derived DCs, when treated with interferon-alpha or lipopolysaccharide during the final 24 hours of culture, expressed an activated phenotype that included up-regulation of MHC class II, CD1d, CD8 alpha, CD80, CD86, and CD40, The FL-derived DCs also exhibited potent antigen-processing and antigen-presenting capacity. Neutralizing anti-interleukin-6 (IL-6) antibody, but not anti-GM-CSF, significantly reduced the number of DCs generated in vitro with FL, suggesting that IL-6 has a role in the development of DCs from BM precursors. Stem cell factor, which exhibits some of the same bioactivities as FL, was unable to replace FL to promote DC development in vitro. This culture system will facilitate detailed analysis of murine DC development. (C) 2000 by The American Society of Hematology.

关键词：抗原 CD/分析抗原 CD86 骨髓细胞/细胞学骨髓细胞/免疫学 CD4阳性T淋巴细胞/细胞学 CD4阳性T淋巴细胞/免疫学细胞培养的树突细胞/细胞学树突细胞/免疫学粒细胞巨噬细胞集落刺激因子/药理学造血干细胞/细胞学造血干细胞/药物作用造血干细胞/免疫学组织相容性抗原Ⅱ类/分析整合素αXβ2/分析白细胞介素12/分析白细胞介素6/缺乏白细胞介素6/遗传学白细胞介素6/生理学白细胞生成/免疫学淋巴细胞培养试验混合膜糖蛋白类/分析小鼠近交BALBC 小鼠近交C57BL 小鼠近交DBA 小鼠基因敲除原癌基因蛋白质类/药理学受体蛋白质酪氨酸激酶类/药理学重组蛋白质类/药理学脾/细胞学脾/免疫学 fms样酪氨酸激酶3 动物女(雌)性人类小鼠

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The development and compensation of biliary cirrhosis in interleukin-6-deficient mice

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AMERICAN JOURNAL OF PATHOLOGY 2000年第5期156卷 1627-1639页

作者： Ezure, T Sakamoto, T Tsuji, H Lunz, JG Murase, N Fung, JJ Demetris, AJ Univ Pittsburgh Med Ctr Thomas E Starzl Transplantat Inst Div Transplantat Pittsburgh PA 15261 USA Univ Pittsburgh Med Ctr Dept Pathol Div Transplantat Pittsburgh PA 15261 USA Univ Pittsburgh Med Ctr Dept Surg Div Transplantat Pittsburgh PA 15261 USA

In an effort to understand the role of IL-6/gp130 signaling In chronic liver injury, IL-6 deficient (IL-6(-/-)) and wild-type control (IL-6(+/+)) mice were subjected to bile duct ligation (BDL) for 12 weeks. This maneuver causes chronic biomechanical stress and liver injury, fueling sustained biliary epithelial and hepatocyte proliferation. By 12 weeks after BDL, IL-6(-/-) mice develop significantly higher total serum bilirubin levels (23.2 +/- 2.3 versus 14.9 +/- 2.1 mg/dl, P < 0.0001;delta bilirubin subfraction 16.7 +/- 4.0% versus 9.2 +/- 1.8%;P < 0.002), and the majority (15/18) show "black" gallbladder bile, compared to IL-6(+/+) mice (5/16;P < 0.003), The IL-6(-/-) mice also cannot sustain the compensatory liver mass increase commonly seen with chronic obstructive cholangiopathy, because of less hepatocyte proliferation, despite a rate of hepatocyte apoptosis similar to that of IL-6(+/+) mice. Moreover, IL-6(-/-) mice show a more advanced stage of biliary fibrosis and a higher mortality rate than the IL-6(+/+) controls (51% versus 23%;P < 0.02). These phenotypic changes in the IL-6(-/-) mice are associated with decreased expression and phosphorylation of gp130 and the transcription factor STAT3, compared to IL-6+/+ mice. Daily treatment with exogenous recombinant IL-6 for 3-6 weeks starting at 6 weeks after BDL significantly lowers the serum total bilirubin in both groups. In the IL-6(-/-) mice, exogenous IL-6 treatment also increases the level of gp130 protein expression and completely reverses the loss of liver mass by increasing the hepatocyte proliferation. In conclusion, IL-6 appears to contribute to biliary tree integrity and maintenance of hepatocyte mass during chronic injury.

关键词：丙氨酸转氨酶/血液抗原 CD/药物作用抗原 CD/代谢细胞凋亡胆汁/化学胆管/外科学胆红素/血液体重细胞分裂细胞因子受体gp130 原位缺口末端标记白细胞介素6/缺乏白细胞介素6/遗传学白细胞介素6/药理学肝/代谢肝/病理学肝硬化胆汁性/病因学肝硬化胆汁性/死亡率肝硬化胆汁性/病理学膜糖蛋白类/药物作用膜糖蛋白类/代谢小鼠突变型器官测量重组蛋白质类/药理学信号传导/药物作用存活率分析动物男(雄)性小鼠

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The residual megakaryocyte and platelet production in c-Mpl-deficient mice is not dependent on the actions of interleukin-6, interleukin-11, or leukemia inhibitory factor

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BLOOD 2000年第2期95卷 528-534页

作者： Gainsford, T Nandurkar, H Metcalf, D Robb, L Begley, CG Alexander, WS Walter & Eliza Hall Inst Med Res Melbourne Vic 3050 Australia Royal Melbourne Hosp Cooperat Res Ctr Cellular Growth Factors Melbourne Vic Australia Royal Melbourne Hosp Rotary Bone Marrow Res Labs Melbourne Vic Australia

Mice lacking thrombopoietin (TPO) or its receptor c-Mpl are severely thrombocytopenic, consistent with a dominant physiological role for this cytokine in megakaryocytopoiesis, However, these mice remain healthy and show no signs of spontaneous hemorrhage, implying that TPO-independent mechanisms for platelet production exist and are sufficient for hemostasis. To investigate the roles of cytokines that act through the gp130 signaling chain in the residual platelet production of mpl(-/-) mice, mpl -/-IL-6(-/-), mpl(-/-)LIF(-/-), and mpl(-/-)IL-11R alpha(-/-) double-mutant mice were generated. In each of these compound mutants, the number of circulating platelets was no lower than that observed in mice lacking only the c-mpl gene. Moreover, the deficits in the numbers of megakaryocytes and megakaryocyte progenitor cells in the bone marrow and spleen were no further exacerbated in mpl(-/-)L-6(-/-), mpl(-/-)LIF(-/-), or mpl(-/-) IL-11R alpha(-/-) double-mutant mice compared, with those in Mpl-deficient animals. In single IL-6(-/-), LIF-/-, and IL-11R alpha(-/-) mutant mice, platelet production was normal. These data establish that, as single regulators, IL-6, IL-11, and LIF have no essential role in normal steady-state megakaryocytopoiesis, and are not required for the residual megakaryocyte and platelet production seen in the c-mpl(-/-) mouse. (Blood, 2000;95:528-534) (C) 2000 by The American Society of Hematology.

关键词：血小板/细胞学骨髓细胞/细胞学基因型生长抑制物/缺乏生长抑制物/遗传学生长抑制物/生理学血细胞生成/遗传学血细胞生成/生理学造血干细胞/细胞学造血干细胞/药物作用造血干细胞/生理学白细胞介素11/缺乏白细胞介素11/遗传学白细胞介素11/生理学白细胞介素6/缺乏白细胞介素6/遗传学白细胞介素6/生理学白血病抑制因子淋巴因子/缺乏淋巴因子/遗传学淋巴因子/生理学巨核细胞/细胞学小鼠基因敲除肿瘤蛋白质类血小板计数原癌基因蛋白质类/缺乏原癌基因蛋白质类/遗传学原癌基因蛋白质类/生理学受体细胞因子受体血小板生成素脾/细胞学血小板生成素/缺乏血小板生成素/遗传学血小板生成素/生理学动物小鼠

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Adenoviral transfer of murine oncostatin M elicits periosteal bone apposition in knee joints of mice, despite synovial inflammation and up-regulated expression of interleukin-6 and receptor activator of nuclear factor-κB ligand

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AMERICAN JOURNAL OF PATHOLOGY 2002年第5期160卷 1733-1743页

作者： de Hooge, ASK van de Loo, FAJ Bennink, MB de Jong, DS Arntz, OJ Lubberts, E Richards, CD van den Berg, WB Univ Nijmegen Med Ctr Ctr Mol Life Sci Rheumatol Res Lab NL-6500 HB Nijmegen Netherlands Catholic Univ Nijmegen Nijmegen Netherlands McMaster Univ Dept Pathol & Mol Med Hamilton ON Canada

Oncostatin M (OSM) has been described as a bone-remodeling factor either stimulating osteoblast activity or osteoclast formation in vitro. To elucidate the in vivo effect of OSM on bone remodeling, we injected an adenoviral vector encoding murine OSM in knee joints of mice. OSM strongly induced interleukin (IL)-6 gene expression, a known mediator of osteoclast development. We investigated the OSM effect in wild-type and IL-6-deficient mice and found a similar degree of OSM-induced joint inflammation. Within the first week of inflammation, the periosteum along the femur and tibia increased in cell number and stained positive for the osteoblast marker alkaline phosphatase. At these sites bone apposition occurred in both strains as demonstrated by Goldner and Von Kossa staining. In vitro OSM enhanced the effect of bone morphogenetic protein-2 on osteoblast differentiation. immunohistochemistry demonstrated expression of receptor activator of nuclear factor-kappaB ligand (RANKL) and its receptor, receptor activator of nuclear factor-kappaB (RANK), in the periosteum but osteoclasts were not detected at sites of bone apposition. Induced mRNA expression for the receptor activator of nuclear factor-kappaB ligand inhibitor osteoprotegerin probably controlled osteoclast development during OSM overexpression. Our results show that OSM favors bone apposition at periosteal sites instead of resorption in vivo. This effect was not dependent on or inhibited by IL-6.

关键词：腺病毒科/遗传学碱性磷酸酶/药物作用碱性磷酸酶/代谢关节炎/遗传学关节炎/病理生理学骨形态发生蛋白质2 骨形态发生蛋白质类/药理学载体蛋白质类/生物合成细胞系剂量效应关系药物基因表达基因转移技术基因型糖蛋白类/生物合成白细胞介素6/生物合成白细胞介素6/缺乏白细胞介素6/药理学膝关节/病理生理学膜糖蛋白类/生物合成小鼠近交C57BL 抑瘤素M 骨生成骨保护素肽类/遗传学肽类/药理学肽类/生理学骨膜/病理生理学 RANK配体核因子κB受体活化因子受体胞质和核/生物合成受体肿瘤坏死因子重组蛋白质类/药理学无特异性病原体有机物滑膜炎/代谢滑膜炎/病理生理学转化生长因子β 增量调节动物男(雄)性小鼠

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