M-CSF和IL-10对人单核细胞表面分子表达的影响

本文采用流式细胞术检测人外周血单核细胞表面CD14、CD2 3、CD6 4、CD11b、CD18、CD2 9表达 ,研究巨噬细胞集落刺激因子 (M CSF )和白细胞介素 (IL ) 10对单核细胞炎症效应和免疫效应功能的影响。结果显示 ,(1)M CSF诱导单核细胞表面CD14及CD2 3分子的表达 (P <0 0 5 )。IL 10抑制CD2 3的表达 ,促进CD6 4的表达 ,并协同M CSF诱导单核细胞CD14的表达 ,拮抗M CSF对CD2 3的诱导作用。M CSF能协同IL 10对单核细胞CD6 4的诱导作用 ;(2 )M CSF能诱导单核细胞表面CD11b及CD18的表达 (P <0 0 5 )。结论 :M CSF通过促进单核细胞表面CD11b、CD18、CD14、CD2 3的表达及协同促进CD6 4的表达而促进单核细胞粘附、炎性渗出、IgG及IgE依赖的细胞杀伤和吞噬功能 ,促进单核 巨噬细胞在炎症反应、体液免疫应答效应阶段发挥效应细胞功能。IL 10通过促进CD6 4的表达 ,增强体液免疫应答效应阶段单核 巨噬细胞的免疫效应功能 ,但通过抑制CD2 3的表达 ,下调IgE介导的体液免疫效应。     

牙周病患者血清细胞因子测定的临床意义

目的：探讨了牙周病患者血清IL-8、IL-10、IL-18和M—CSF检测的临床意义。方法：应用放射免疫分析和酶联免疫法对55例牙周病患者进行了治疗前后血清IL-8、IL-10、IL-18和M-CSF水平检测，并与35名正常健康人作比较。结果：牙周病患者在治疗前血清IL-8、IL-10、IL-18和M-CSF水平均非常显著地高于正常人组（P〈0．01），经治疗后-个月，与正常人组比较仍有显著性差异（P〈0．05）。结论：细胞因子IL-8、几-10、几-18和M-CSF在牙周病的发生、发展过程中相互作用，观察其浓度的变化对探讨其发病机理、预防和指导用药均有重要价值。     

急性颅脑损伤患者治疗前后血清GM-CSF、IL-8、hs-CRP联检的临床意义

目的：探讨了急性颅脑损伤患者治疗前后血清GM-CSF、IL-8和hs-CRP水平的变化及意义。方法：应用放射免疫分析和免疫分析对31例急性颅脑损伤患者进行了血清GM-CSF、IL-8和hs-CRP水平测定,并与35名正常健康人作比较。结果：在治疗前急性颅脑损伤患者血清GM-CSF、IL-8和hs-CRP水平均非常显著地高于正常人组（P〈0.01）,经两周治疗后则与正常人比较无显著性差异（P〉0.05）。结论：检测急性颅脑损伤患者血清GM-CSF、IL-8和hs-CRP水平的变化对了解病情、判断疗效和预后观察均具有重要临床价值。     

Increased macrophage colony-stimulating factor levels in patients with Graves’ disease

Previous studies have found markedly elevated serum concentrations of proinflammatory cytokines in patients with Graves’ disease (GD). We investigated the role of macrophage colony-stimulating factor (M-CSF) in GD. We assayed concentrations of M-CSF in sera from 32 patients with GD (25 untreated; 7 receiving thiamazole therapy). We also studied 32 age-matched healthy subjects as controls. Relationships between serum M-CSF and both thyroid state and serum lipids were examined. Moreover, to examine the effect of thyroid hormone alone on serum M-CSF, T3 was administered orally to normal subjects. Serum concentrations of M-CSF in GD patients who were hyperthyroid were significantly increased compared with GD patients who were euthyroid (P < 0.05) and control subjects (P < 0.0001). Serum M-CSF concentrations correlated closely with T3 levels in patients (r = 0.51, P < 0.005). Serial measurement of five individual patients revealed that serum concentrations of M-CSF were significantly decreased (P < 0.05), reaching normal control values upon attainment of euthyroidism. Furthermore, oral T3 administered to 15 volunteers for 7 days produced significant increases in serum levels of M-CSF (P < 0.05). The close correlation between serum M-CSF and serum thyroid hormone levels suggests that high circulating levels of thyroid hormones may directly or indirectly potentiate the production of M-CSF in patients with GD.     

PDGF Receptor Signaling in Osteoblast Lineage Cells Controls Bone Resorption Through Upregulation of Csf1 Expression

The physiological functions of platelet-derived growth factor receptors (PDGFRs) α and β in osteoblast biology and bone metabolism remain to be established. Here, we show that PDGFRA and PDGFRB genes are expressed by osteoblast-lineage canopy and reversal cells in close proximity to PDGFB-expressing osteoclasts within human trabecular bone remodeling units. We also report that, although removal of only one of the two PDGFRs in Osterix-positive cells does not affect bone phenotype, suppression of both PDGFRs in those osteoblast lineage cells increases trabecular bone volume in male mice as well as in female gonad-intact and ovariectomized mice. Furthermore, osteoblast lineage-specific suppression of PDGFRs reduces Csf1 expression, bone marrow level of macrophage colony-stimulating factor (M-CSF), number of osteoclasts, and, therefore, bone resorption, but does not change bone formation. Finally, abrogation of PDGFR signaling in osteoblasts blocks PDGF-induced ERK1/2-mediated Csf1 expression and M-CSF secretion in osteoblast cultures and calcitriol-mediated osteoclastogenesis in co-cultures. In conclusion, our results indicate that PDGFR signaling in osteoblast lineage cells controls bone resorption through ERK1/2-mediated Csf1 expression. © 2020 American Society for Bone and Mineral Research (ASBMR).     

Progression of clinical tuberculosis is associated with a Th2 immune response signature in combination with elevated levels of SOCS3

In this study, we explored the local cytokine/chemokine profiles in patients with active pulmonary or pleural tuberculosis (TB) using multiplex protein analysis of bronchoalveolar lavage and pleural fluid samples. Despite increased pro-inflammation compared to the uninfected controls; there was no up-regulation of IFN-γ or the T cell chemoattractant CCL5 in the lung of patients with pulmonary TB. Instead, elevated levels of IL-4 and CCL4 were associated with high mycobacteria-specific IgG titres as well as SOCS3 (suppressors of cytokine signaling) mRNA and progression of moderate-to-severe disease. Contrary, IL-4, CCL4 and SOCS3 remained low in patients with extrapulmonary pleural TB, while IFN-γ, CCL5 and SOCS1 were up-regulated. Both SOCS molecules were induced in human macrophages infected with Mycobacterium tuberculosis in vitro. The Th2 immune response signature found in patients with progressive pulmonary TB could result from inappropriate cytokine/chemokine responses and excessive SOCS3 expression that may represent potential targets for clinical TB management.     

The prognostic value of intraepithelial and stromal innate immune system cells in non-small cell lung carcinoma

Aims:  The major value of prognostic markers in potentially curable non-small cell lung carcinoma (NSCLC) should be to guide therapy after surgical resection. The prognostic significance of tumour-infiltrating macrophages, their growth factor, macrophage colony-stimulating factor (M-CSF), and its receptor, colony-stimulating factor-1 receptor (CSF-1R), as well as natural killer cells and dendritic cells, is controversial. The aim of this study was to elucidate the prognostic significance of these markers in the epithelial and stromal compartments of NSCLC.
Methods and results:  Tissue microarrays from 335 resected NSCLC, stage I–IIIA were constructed from duplicate cores of epithelial and stromal areas. Immunohistochemistry was used to evaluate epithelial and stromal areas for CD68, M-CSF, CSF-1R, CD56 and CD1a. On univariate analysis, increasing numbers of stromal CD1a+ ( P  = 0.011) and CD56+ cells ( P  = 0.014) correlated significantly with improved disease-specific survival (DSS). On multivariate analysis, stromal CD56+ cells were an independent prognostic factor for DSS (hazard ratio = 2.3, confidence interval = 1.1, 5.0, P  = 0.031).
Conclusions:  High density of stromal CD56+ cells is an independent factor associated with improved prognosis in resected NSCLC, suggesting that these cells mediate an antitumour immune response in the tumour stroma.