搜索结果: 'methocult media formulations for human hematopoietic cells serum containing'

Podar K et al. (FEB 2003) The Journal of biological chemistry 278 8 5794--801

Essential role of caveolae in interleukin-6- and insulin-like growth factor I-triggered Akt-1-mediated survival of multiple myeloma cells.

Caveolae,specialized flask-shaped lipid rafts on the cell surface,are composed of cholesterol,sphingolipids,and structural proteins termed caveolins; functionally,these plasma membrane microdomains have been implicated in signal transduction and transmembrane transport. In the present study,we examined the role of caveolin-1 in multiple myeloma cells. We show for the first time that caveolin-1,which is usually absent in blood cells,is expressed in multiple myeloma cells. Analysis of myeloma cell-derived plasma membrane fractions shows that caveolin-1 is co-localized with interleukin-6 receptor signal transducing chain gp130 and with insulin-like growth factor-I receptor. Cholesterol depletion by beta-cyclodextrin results in the loss of caveola structure in myeloma cells,as shown by transmission electron microscopy,and loss of caveolin-1 function. Interleukin-6 and insulin-like growth factor-I,growth and survival factors in multiple myeloma,induce caveolin-1 phosphorylation,which is abrogated by pre-treatment with beta-cyclodextrin. Importantly,inhibition of caveolin-1 phosphorylation blocks both interleukin-6-induced protein complex formation with caveolin-1 and downstream activation of the phosphatidylinositol 3-kinase/Akt-1 pathway. beta-Cyclodextrin also blocks insulin-like growth factor-I-induced tyrosine phosphorylation of insulin-responsive substrate-1 and downstream activation of the phosphatidylinositol 3-kinase/Akt-1 pathway. Therefore,cholesterol depletion by beta-cyclodextrin abrogates both interleukin-6- and insulin-like growth factor-I-triggered multiple myeloma cell survival via negative regulation of caveolin-1. Taken together,this study identifies caveolin-1 and other structural membrane components as potential new therapeutic targets in multiple myeloma. View Publication

产品类型：

产品号#：

15129

15169

产品名：

RosetteSep™人多发性骨髓瘤细胞富集抗体混合物

Fuertes MB et al. (APR 2008) Journal of immunology (Baltimore,Md. : 1950) 180 7 4606--14

Intracellular retention of the NKG2D ligand MHC class I chain-related gene A in human melanomas confers immune privilege and prevents NK cell-mediated cytotoxicity.

Most tumors grow in immunocompetent hosts despite expressing NKG2D ligands (NKG2DLs) such as the MHC class I chain-related genes A and B (MICA/B). However,their participation in tumor cell evasion is still not completely understood. Here we demonstrate that several human melanomas (cell lines and freshly isolated metastases) do not express MICA on the cell surface but have intracellular deposits of this NKG2DL. Susceptibility to NK cell-mediated cytotoxicity correlated with the ratio of NKG2DLs to HLA class I molecules but not with the amounts of MICA on the cell surface of tumor cells. Transfection-mediated overexpression of MICA restored cell surface expression and resulted in an increased in vitro cytotoxicity and IFN-gamma secretion by human NK cells. In xenografted nude mice,these melanomas exhibited a delayed growth and extensive in vivo apoptosis. Retardation of tumor growth was due to NK cell-mediated antitumor activity against MICA-transfected tumors,given that this effect was not observed in NK cell-depleted mice. Also,mouse NK cells killed MICA-overexpressing melanomas in vitro. A mechanistic analysis revealed the retention of MICA in the endoplasmic reticulum,an effect that was associated with accumulation of endoH-sensitive (immature) forms of MICA,retrograde transport to the cytoplasm,and degradation by the proteasome. Our study identifies a novel strategy developed by melanoma cells to evade NK cell-mediated immune surveillance based on the intracellular sequestration of immature forms of MICA in the endoplasmic reticulum. Furthermore,this tumor immune escape strategy can be overcome by gene therapy approaches aimed at overexpressing MICA on tumor cells. View Publication

产品类型：

产品号#：

15025

15065

产品名：

RosetteSep™人NK细胞富集抗体混合物

O'Mahony L et al. (APR 2006) American journal of physiology. Gastrointestinal and liver physiology 290 4 G839--45

Differential cytokine response from dendritic cells to commensal and pathogenic bacteria in different lymphoid compartments in humans.

Resident host microflora condition and prime the immune system. However,systemic and mucosal immune responses to bacteria may be divergent. Our aim was to compare,in vitro,cytokine production by human mononuclear and dendritic cells (DCs) from mesenteric lymph nodes (MLNs) and peripheral blood mononuclear cells (PBMCs) to defined microbial stimuli. Mononuclear cells and DCs isolated from the MLN (n = 10) and peripheral blood (n = 12) of patients with active colitis were incubated in vitro with the probiotic bacteria Lactobacillus salivarius UCC118 or Bifidobacterium infantis 35624 or the pathogenic organism Salmonella typhimurium UK1. Interleukin (IL)-12,tumor necrosis factor (TNF)-alpha,transforming growth factor (TGF)-beta,and IL-10 cytokine levels were quantified by ELISA. PBMCs and PBMC-derived DCs secreted TNF-alpha in response to the Lactobacillus,Bifidobacteria,and Salmonella strains,whereas MLN cells and MLN-derived DCs secreted TNF-alpha only in response to Salmonella challenge. Cells from the systemic compartment secreted IL-12 after coincubation with Salmonella or Lactobacilli,whereas MLN-derived cells produced IL-12 only in response to Salmonella. PBMCs secreted IL-10 in response to the Bifidobacterium strain but not in response to the Lactobacillus or Salmonella strain. However,MLN cells secreted IL-10 in response to Bifidobacteria and Lactobacilli but not in response to Salmonella. In conclusion,commensal bacteria induced regulatory cytokine production by MLN cells,whereas pathogenic bacteria induce T cell helper 1-polarizing cytokines. Commensal-pathogen divergence in cytokine responses is more marked in cells isolated from the mucosal immune system compared with PBMCs. View Publication

产品类型：

产品号#：

09600

09650

产品名：

StemSpan™ SFEM

Bhattacharyya S et al. (AUG 2004) Blood 104 4 1100--9

Immunoregulation of dendritic cells by IL-10 is mediated through suppression of the PI3K/Akt pathway and of IkappaB kinase activity.

Interleukin-10 (IL-10) has potent immunoregulatory effects on the maturation and the antigen-presenting cell (APC) function of dendritic cells (DCs). The molecular basis underlying these effects in DCs,however,is ill defined. It is well established that the transcription factor NF-kappaB is a key regulator of DC development,maturation,and APC function. This study was initiated to determine the effects of IL-10 on the NF-kappaB signaling pathway in immature DCs. IL-10 pretreatment of myeloid DCs cultured from bone marrow resulted in reduced DNA binding and nuclear translocation of NF-kappaB after anti-CD40 antibody or lipopolysaccharide (LPS) stimulation. Furthermore,inhibited NF-kappaB activation was characterized by reduced degradation,phosphorylation,or both of IkappaBalpha and IkappaBepsilon but not IkappaBbeta and by reduced phosphorylation of Ser536,located in the trans-activation domain of p65. Notably,IL-10-mediated inhibition of NF-kappaB coincided with suppressed IkappaB kinase (IKK) activity in vitro. Furthermore,IL-10 blocked inducible Akt phosphorylation,and inhibitors of phosphatidylinositol 3-kinase (PI3K) effectively suppressed the activation of Akt,IKK,and NF-kappaB. These findings demonstrate that IL-10 targets IKK activation in immature DCs and that suppressing the PI3K pathway in part mediates blockade of the pathway. View Publication

产品类型：

产品号#：

18758

18758RF

18768

18768RF

产品名：

N. J. Ronaghan et al. ( 2022) PloS one 17 10 e0276013

M1-like, but not M0- or M2-like, macrophages, reduce RSV infection of primary bronchial epithelial cells in a media-dependent fashion.

Respiratory syncytial virus (RSV) is a common childhood infection that in young infants can progress into severe bronchiolitis and pneumonia. Disease pathogenesis results from both viral mediated and host immune processes of which alveolar macrophages play an important part. Here,we investigated the role of different types of alveolar macrophages on RSV infection using an in vitro co-culture model involving primary tissue-derived human bronchial epithelial cells (HBECs) and human blood monocyte-derived M0-like,M1-like,or M2-like macrophages. It was hypothesized that the in vitro model would recapitulate previous in vivo findings of a protective effect of macrophages against RSV infection. It was found that macrophages maintained their phenotype for the 72-hour co-culture time period and the bronchial epithelial cells were unaffected by the macrophage media. HBEC infection with RSV was decreased by M1-like macrophages but enhanced by M0- or M2-like macrophages. The medium used during the co-culture also impacted the outcome of the infection. This work demonstrates that alveolar macrophage phenotypes may have differential roles during epithelial RSV infection,and demonstrates that an in vitro co-culture model could be used to further investigate the roles of macrophages during bronchial viral infection. View Publication

产品类型：

产品号#：

05040

100-1079

19359

产品名：

PneumaCult™-Ex Plus 培养基

EasySep™ 总核酸提取试剂盒

EasySep™人单核细胞分选试剂盒

产品手册

RoboSep™: Solutions for HIV Research

产品类型：

品牌：

RoboSep

产品号#：

17851

17851RF

17852

17852RF

17853

17853RF

17854

17854RF

17951

17951RF

17952

17952RF

17953

17953RF

18051

18051RF

18052

18052RF

18053

18053RF

18054

18054RF

19155

19155RF

19158

19158RF

19159

19159RF

19254

19254RF

19264

19555

19555RF

19661

19662

19663

19051

1

产品名：

EasySep™人CD3正选试剂盒II

RoboSep™ 人CD3正选试剂盒II

EasySep™人CD4正选试剂盒II

RoboSep™ 人CD4正选试剂盒II

EasySep™人CD8正选试剂盒 II

RoboSep™ 人CD8正选试剂盒 II

EasySep™人CD19正选试剂盒II

RoboSep™ 人CD19正选试剂盒II

EasySep™人T细胞分选试剂盒

RoboSep™ 人T细胞分选试剂盒

EasySep™人CD4+ T细胞分选试剂盒

RoboSep™ 人CD4+ T细胞分选试剂盒

EasySep™人CD8+ T细胞分选试剂盒

RoboSep™ 人CD8+ T细胞分选试剂盒

EasySep™人记忆CD8+ T细胞富集试剂盒

RoboSep™ 人记忆CD8+ T细胞富集试剂盒

EasySep™人Naïve B细胞富集试剂盒

RoboSep™ 人Naïve B细胞富集试剂盒含滤芯吸头

EasySep™ Direct 人Naïve B细胞分选试剂盒

EasySep™人Naïve CD4+ T细胞分选试剂盒

RoboSep™ 人Naïve CD4+ T细胞分选试剂盒

EasySep™ Direct人T细胞分选试剂盒

EasySep™ Direct人CD4+ T细胞分选试剂盒

EasySep™ Direct人CD8+ T细胞分选试剂盒

EasySep™人T细胞富集试剂盒

CellPore™: For Gentle Intracellular Delivery

1:54

视频

CellPore™: For Gentle Intracellular Delivery

发布日期: 10/10/24

S. Gupta et al. ( 2018) Immunity & ageing : I & A 15 2

Molecular changes associated with increased TNF-?-induced apoptotis in naive (TN) and central memory (TCM) CD8+ T cells in aged humans.

Background Progressive T cell decline in aged humans is associated with a deficiency of naive (TN) and central memory (TCM) T cells. We have previously reported increased tumor necrosis factor-? (TNF-?)-induced apoptosis in TN and TCM T cells in aged humans; however,the molecular basis of increased apoptosis remains to be defined. Since expression of TNF receptors (TNFRs) was reported to be comparable in young and aged,we investigated signaling events downstream of TNFRs to understand the molecular basis of increased TNF-?-induced apoptosis in aged TN and TCM CD8+ cells. Results The expression of TRAF-2 and RIP,phosphorylation of JNK,IKK?/?,and I?B?,and activation of NF-?B activation were significantly decreased in TN and TCM CD8+ cells from aged subjects as compared to young controls. Furthermore,expression of A20,Bcl-xL,cIAP1,and FLIP-L and FLIP-S was significantly decreased in TN and TCM CD8+ cells from aged subjects. Conclusions These data demonstrate that an impaired expression/function of molecules downstream TNFR signaling pathway that confer survival signals contribute to increased apoptosis of TN and TCM CD8+ cells in aged humans. View Publication

产品类型：

产品号#：

17654

产品名：

EasySep™ Release人PE正选试剂盒

产品手册

Reliable Antibodies for Your Research

产品类型：

品牌：

EasySep

产品号#：

60100

60100.1

60100AD

60100AD.1

60102

60102FI

60104

60104AD

60104AD.1

60104AZ

60104AZ.1

60104BT

60104BT.1

60104BT.2

60104FI

60104FI.1

60104PE

60104PE.1

60106

60106.1

60106AZ

60106AZ.1

60106BT

60106BT.1

60106FI

60106FI.1

60106PE

60106PE.1

60107

60107.1

601

产品名：

抗β-微管蛋白III抗体，克隆AA10

抗β-微管蛋白III抗体，克隆AA10，Alexa Fluor® 488

抗β-微管蛋白III抗体，clone AA10，Alexa Fluor® 488

抗小鼠TCR Gamma/Delta抗体，clone GL3

抗小鼠TCR Gamma/Delta抗体，clone GL3，Alexa Fluor® 488

抗小鼠TCR Gamma/Delta抗体，clone GL3，APC

抗小鼠TCR Gamma/Delta抗体，clone GL3，Biotin

抗小鼠TCR Gamma/Delta抗体，clone GL3，FITC

抗小鼠TCR Gamma/Delta抗体，clone GL3，PE

抗人CD71（转铁蛋白受体）抗体，clone OKT9

抗人CD71（转铁蛋白受体）抗体，clone OKT9，APC

抗人CD71（转铁蛋白受体）抗体，clone OKT9，Biotin

抗人CD71（转铁蛋白受体）抗体，clone OKT9，FITC

抗人CD71（转铁蛋白受体）抗体，clone OKT9，PE

Kortylewski M et al. (DEC 2005) Nature medicine 11 12 1314--21

Inhibiting Stat3 signaling in the hematopoietic system elicits multicomponent antitumor immunity.

The immune system can act as an extrinsic suppressor of tumors. Therefore,tumor progression depends in part on mechanisms that downmodulate intrinsic immune surveillance. Identifying these inhibitory pathways may provide promising targets to enhance antitumor immunity. Here,we show that Stat3 is constitutively activated in diverse tumor-infiltrating immune cells,and ablating Stat3 in hematopoietic cells triggers an intrinsic immune-surveillance system that inhibits tumor growth and metastasis. We observed a markedly enhanced function of dendritic cells,T cells,natural killer (NK) cells and neutrophils in tumor-bearing mice with Stat3(-/-) hematopoietic cells,and showed that tumor regression requires immune cells. Targeting Stat3 with a small-molecule drug induces T cell- and NK cell-dependent growth inhibition of established tumors otherwise resistant to direct killing by the inhibitor. Our findings show that Stat3 signaling restrains natural tumor immune surveillance and that inhibiting hematopoietic Stat3 in tumor-bearing hosts elicits multicomponent therapeutic antitumor immunity. View Publication

产品类型：

产品号#：

18709

18709RF

产品名：

EasySep™小鼠定制正选试剂盒

RoboSep™ 小鼠定制正选试剂盒含滤芯吸头

Hidalgo A et al. (JAN 2005) Blood 105 2 567--75

Enforced fucosylation of neonatal CD34+ cells generates selectin ligands that enhance the initial interactions with microvessels but not homing to bone marrow.

Hematopoietic progenitor/stem cell homing to the bone marrow requires the concerted action of several adhesion molecules. Endothelial P- and E-selectins play an important role in this process,but their ligands on a large subset of neonate-derived human CD34+ cells are absent,leading to a reduced ability to interact with the bone marrow (BM) microvasculature. We report here that this deficiency results from reduced alpha1,3-fucosyltransferase (FucT) expression and activity in these CD34+ cells. Incubation of CD34+ cells with recombinant human FucTVI rapidly corrected the deficiency in nonbinding CD34+ cells and further increased the density of ligands for both P- and E-selectins on all cord blood-derived CD34+ cells. Intravital microscopy studies revealed that these FucTVI-treated CD34+ cells displayed a marked enhancement in their initial interactions with the BM microvasculature,but unexpectedly,homing into the BM was not improved by FucTVI treatment. These data indicate that,although exogenous FucT enzyme activity can rapidly modulate selectin binding avidity of cord blood CD34+ cells,further studies are needed to understand how to translate a positive effect on progenitor cell adhesion in bone marrow microvessels into one that significantly influences migration and lodgement into the parenchyma. View Publication

产品类型：

产品号#：

18056

18056RF

产品名：

S. Jaleco et al. (7 2003) The Journal of Immunology 171 61-68

Homeostasis of Naive and Memory CD4 + T Cells: IL-2 and IL-7 Differentially Regulate the Balance Between Proliferation and Fas-Mediated Apoptosis

Cytokines play a crucial role in the maintenance of polyclonal naive and memory T cell populations. It has previously been shown that ex vivo,the IL-7 cytokine induces the proliferation of naive recent thymic emigrants (RTE) isolated from umbilical cord blood but not mature adult-derived naive and memory human CD4(+) T cells. We find that the combination of IL-2 and IL-7 strongly promotes the proliferation of RTE,whereas adult CD4(+) T cells remain relatively unresponsive. Immunological activity is controlled by a balance between proliferation and apoptotic cell death. However,the relative contributions of IL-2 and IL-7 in regulating these processes in the absence of MHC/peptide signals are not known. Following exposure to either IL-2 or IL-7 alone,RTE,as well as mature naive and memory CD4(+) T cells,are rendered only minimally sensitive to Fas-mediated cell death. However,in the presence of the two cytokines,Fas engagement results in a high level of caspase-dependent apoptosis in both RTE as well as naive adult CD4(+) T cells. In contrast,equivalently treated memory CD4(+) T cells are significantly less sensitive to Fas-induced cell death. The increased susceptibility of RTE and naive CD4(+) T cells to Fas-induced apoptosis correlates with a significantly higher IL-2/IL-7-induced Fas expression on these T cell subsets than on memory CD4(+) T cells. Thus,IL-2 and IL-7 regulate homeostasis by modulating the equilibrium between proliferation and apoptotic cell death in RTE and mature naive and memory T cell subsets. View Publication

产品类型：

产品号#：

15023

产品名：

RosetteSep™ 人CD8+ T细胞富集抗体混合物

搜索结果: 'methocult media formulations for human hematopoietic cells serum containing'

Essential role of caveolae in interleukin-6- and insulin-like growth factor I-triggered Akt-1-mediated survival of multiple myeloma cells.

Intracellular retention of the NKG2D ligand MHC class I chain-related gene A in human melanomas confers immune privilege and prevents NK cell-mediated cytotoxicity.

Differential cytokine response from dendritic cells to commensal and pathogenic bacteria in different lymphoid compartments in humans.

Immunoregulation of dendritic cells by IL-10 is mediated through suppression of the PI3K/Akt pathway and of IkappaB kinase activity.

M1-like, but not M0- or M2-like, macrophages, reduce RSV infection of primary bronchial epithelial cells in a media-dependent fashion.

Molecular changes associated with increased TNF-?-induced apoptotis in naive (TN) and central memory (TCM) CD8+ T cells in aged humans.

Inhibiting Stat3 signaling in the hematopoietic system elicits multicomponent antitumor immunity.

Enforced fucosylation of neonatal CD34+ cells generates selectin ligands that enhance the initial interactions with microvessels but not homing to bone marrow.

Homeostasis of Naive and Memory CD4 + T Cells: IL-2 and IL-7 Differentially Regulate the Balance Between Proliferation and Fas-Mediated Apoptosis

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