Human Peripheral Blood Mononuclear Cells, Frozen

Primary human cells, frozen
From: 129 USD


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Primary human cells, frozen
From: 129 USD


Primary human mononuclear cells (MNCs) were isolated from peripheral blood (PB) leukapheresis or whole blood samples using density gradient separation or red blood cell lysis. PB was collected using acid-citrate-dextrose solution A (ACDA), acid-citrate-dextrose solution B (ACDB), citrate-phosphate-dextrose (CPD), or sodium heparin (Na-Hep) as the anticoagulant.

Cells were obtained using Institutional Review Board (IRB)-approved consent forms and protocols.

Standard PBMCs (Catalog #70025) include the following characterization criteria: cell count, viability, donor virus testing, age, sex, ethnicity, weight, height and smoking status.

Characterized PBMCs (Catalog #70047) include the same information as Standard PBMCs in addition to the following characterization criteria: high-resolution HLA typing (A, B, C, DRB1, DRB3/4/5 and DQB1), ADCC status, ELISpot reactivity and cell proliferation index.

HLA-A2 PBMCs (Catalog #70048) are selected for HLA-A2 positive donors and include the same characterization criteria as Standard PBMCs and Characterized PBMCs.

Certain products are only available in select territories. Please contact your local Sales representative or Product & Scientific Support at for further information.
• CryoStor® CS10 (Catalog #70025) or
• Serum-free cryopreservation medium and 10% dimethyl sulfoxide (DMSO) (Catalog #70047 and #70048)
Cell Type:
Mononuclear Cells
Cell and Tissue Source:
Peripheral Blood
Donor Status:

Scientific Resources

Educational Materials


Data and Publications


Journal of biotechnology 2016 MAY

A novel approach for emerging and antibiotic resistant infections: Innate defense regulators as an agnostic therapy.

North JR et al.


Innate Defense Regulators (IDRs) are short synthetic peptides that target the host innate immune system via an intracellular adaptor protein which functions at key signaling nodes. In this work, further details of the mechanism of action of IDRs have been discovered. The studies reported here show that the lead clinical IDR, SGX94, has broad-spectrum activity against Gram-negative and Gram-positive bacterial infections caused by intracellular or extracellular bacteria and also complements the actions of standard of care antibiotics. Based on in vivo and primary cell culture studies, this activity is shown to result from the primary action of SGX94 on tissue-resident cells and subsequent secondary signaling to activate myeloid-derived cells, resulting in enhanced bacterial clearance and increased survival. Data from non-clinical and clinical studies also show that SGX94 treatment modulates pro-inflammatory and anti-inflammatory cytokine levels, thereby mitigating the deleterious inflammatory consequences of innate immune activation. Since they act through host pathways to provide both broad-spectrum anti-infective capability as well as control of inflammation, IDRs are unlikely to be impacted by resistance mechanisms and offer potential clinical advantages in the fight against emerging and antibiotic resistant bacterial infections.
Organic & biomolecular chemistry 2016 JUL

Cellular thermal shift and clickable chemical probe assays for the determination of drug-target engagement in live cells.

Xu H et al.


Proof of drug-target engagement in physiologically-relevant contexts is a key pillar of successful therapeutic target validation. We developed two orthogonal technologies, the cellular thermal shift assay (CETSA) and a covalent chemical probe reporter approach (harnessing sulfonyl fluoride tyrosine labeling and subsequent click chemistry) to measure the occupancy of the mRNA-decapping scavenger enzyme DcpS by a small molecule inhibitor in live cells. Enzyme affinity determined using isothermal dose response fingerprinting (ITDRFCETSA) and the concentration required to occupy 50% of the enzyme (OC50) using the chemical probe reporter assay were very similar. In this case, the chemical probe method worked well due to the long offset kinetics of the reversible inhibitor (determined using a fluorescent dye-tagged probe). This work suggests that CETSA could become the first choice assay to determine in-cell target engagement due to its simplicity.
Analytical chemistry 2016 APR

Water-in-Water Droplets by Passive Microfluidic Flow Focusing.

Moon B-U et al.


We present a simple microfluidic system that generates water-in-water, aqueous two phase system (ATPS) droplets, by passive flow focusing. ATPS droplet formation is achieved by applying weak hydrostatic pressures, with liquid-filled pipette tips as fluid columns at the inlets, to introduce low speed flows to the flow focusing junction. To control the size of the droplets, we systematically vary the interfacial tension and viscosity of the ATPS fluids and adjust the fluid column height at the fluid inlets. The size of the droplets scales with a power law of the ratio of viscous stresses in the two ATPS phases. Overall, we find a drop size coefficient of variation (CV; i.e., polydispersity) of about 10%. We also find that when drops form very close to the flow focusing junction, the drops have a CV of less than 1%. Our droplet generation method is easily scalable: we demonstrate a parallel system that generates droplets simultaneously and improves the droplet production rate by up to one order of magnitude. Finally, we show the potential application of our system for encapsulating cells in water-in-water emulsions by encapsulating microparticles and cells. To the best of our knowledge, our microfluidic technique is the first that forms low interfacial tension ATPS droplets without applying external perturbations. We anticipate that this simple approach will find utility in drug and cell delivery applications because of the all-biocompatible nature of the water-in-water ATPS environment.
Frontiers in cellular and infection microbiology 2015 DEC

Mycobacterium tuberculosis Infection Induces HDAC1-Mediated Suppression of IL-12B Gene Expression in Macrophages.

Chandran A et al.


Downregulation of host gene expression is one of the many strategies employed by intracellular pathogens such as Mycobacterium tuberculosis (MTB) to survive inside the macrophages and cause disease. The underlying molecular mechanism behind the downregulation of host defense gene expression is largely unknown. In this study we explored the role of histone deacetylation in macrophages in response to infection by virulent MTB H37Rv in manipulating host gene expression. We show a significant increase in the levels of HDAC1 with a concomitant and marked reduction in the levels of histone H3-acetylation in macrophages containing live, but not killed, virulent MTB. Additionally, we show that HDAC1 is recruited to the promoter of IL-12B in macrophages infected with live, virulent MTB, and the subsequent hypoacetylation of histone H3 suppresses the expression of this gene which plays a key role in initiating Th1 responses. By inhibiting immunologically relevant kinases, and by knockdown of crucial transcriptional regulators, we demonstrate that protein kinase-A (PKA), CREB, and c-Jun play an important role in regulating HDAC1 level in live MTB-infected macrophages. By chromatin immunoprecipitation (ChIP) analysis, we prove that HDAC1 expression is positively regulated by the recruitment of c-Jun to its promoter. Knockdown of HDAC1 in macrophages significantly reduced the survival of intracellular MTB. These observations indicate a novel HDAC1-mediated epigenetic modification induced by live, virulent MTB to subvert the immune system to survive and replicate in the host.
Applied and environmental microbiology 2013 MAR

Identification of one novel candidate probiotic Lactobacillus plantarum strain active against influenza virus infection in mice by a large-scale screening.

Kechaou N et al.


In this study, we developed a large-scale screening of bacterial strains in order to identify novel candidate probiotics with immunomodulatory properties. For this, 158 strains, including a majority of lactic acid bacteria (LAB), were screened by two different cellular models: tumor necrosis factor alpha (TNF-α)-activated HT-29 cells and peripheral blood mononuclear cells (PBMCs). Different strains responsive to both models (pro- and anti-inflammatory strains) were selected, and their protective effects were tested in vivo in a murine model of influenza virus infection. Daily intragastric administrations during 10 days before and 10 days after viral challenge (100 PFU of influenza virus H1N1 strain A Puerto Rico/8/1934 [A/PR8/34]/mouse) of Lactobacillus plantarum CNRZ1997, one potentially proinflammatory probiotic strain, led to a significant improvement in mouse health by reducing weight loss, alleviating clinical symptoms, and inhibiting significantly virus proliferation in lungs. In conclusion, in this study, we have combined two cellular models to allow the screening of a large number of LAB for their immunomodulatory properties. Moreover, we identified a novel candidate probiotic strain, L. plantarum CNRZ1997, active against influenza virus infection in mice.
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