Human Peripheral Blood Leukopak, Fresh

Primary human cells, fresh

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Primary human cells, fresh
From: 829 USD

Overview

Leukopaks are an enriched leukapheresis product consisting of a large number of single-donor mononuclear cells (MNCs) collected from normal peripheral blood. Leukapheresis is performed on normal donors using Institutional Review Board (IRB)-approved consent forms and protocols. Approximately two to three blood volumes are processed using the Spectra Optia® Apheresis System (unless otherwise requested) to produce a full-sized Leukopak. Acid citrate dextrose, solution A (ACDA) is the anticoagulant. High-resolution HLA typing for Class I and Class II alleles and CMV status are available upon request.

Certain products are only available in select territories. Please contact your local Sales representative or Product & Scientific Support at techsupport@stemcell.com for further information and to inquire about donor selection or information including BMI category, smoking status, ethnicity, etc.

Browse our Frequently Asked Questions (FAQs) on Primary Cells.
Subtype:
Fresh
Cell Type:
Leukopak; Mononuclear Cells
Species:
Human
Cell and Tissue Source:
Peripheral Blood
Donor Status:
Normal

Scientific Resources

Product Documentation

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Educational Materials

(4)

Data and Publications

Publications

(3)
Cell systems 2020 mar

Gut-Liver Physiomimetics Reveal Paradoxical Modulation of IBD-Related Inflammation by Short-Chain Fatty Acids.

M. Trapecar et al.

Abstract

Although the association between the microbiome and IBD and liver diseases is known, the cause and effect remain elusive. By connecting human microphysiological systems of the gut, liver, and circulating Treg and Th17 cells, we created a multi-organ model of ulcerative colitis (UC) ex vivo. The approach shows microbiome-derived short-chain fatty acids (SCFAs) to either improve or worsen UC severity, depending on the involvement of effector CD4 T cells. Using multiomics, we found SCFAs increased production of ketone bodies, glycolysis, and lipogenesis, while markedly reducing innate immune activation of the UC gut. However, during acute T cell-mediated inflammation, SCFAs exacerbated CD4+ T cell-effector function, partially through metabolic reprograming, leading to gut barrier disruption and hepatic injury. These paradoxical findings underscore the emerging utility of human physiomimetic technology in combination with systems immunology to study causality and the fundamental entanglement of immunity, metabolism, and tissue homeostasis.
Science advances 2020 jun

Impact of mRNA chemistry and manufacturing process on innate immune activation.

J. Nelson et al.

Abstract

Messenger RNA (mRNA) represents an attractive therapeutic modality for potentially a wide range of clinical indications but requires uridine chemistry modification and/or tuning of the production process to prevent activation of cellular innate immune sensors and a concomitant reduction in protein expression. To decipher the relative contributions of these factors on immune activation, here, we compared, in multiple cell and in vivo models, mRNA that encodes human erythropoietin incorporating either canonical uridine or N1-methyl-pseudouridine (1m$\Psi$), synthesized by either a standard process shown to have double-stranded RNA (dsRNA) impurities or a modified process that yields a highly purified mRNA preparation. Our data demonstrate that the lowest stimulation of immune endpoints was with 1m$\Psi$ made by the modified process, while mRNA containing canonical uridine was immunostimulatory regardless of process. These findings confirm that uridine modification and the reduction of dsRNA impurities are both necessary and sufficient at controlling the immune-activating profile of therapeutic mRNA.
Biotechnology and bioengineering 2017

Integrated gut/liver microphysiological systems elucidates inflammatory inter-tissue crosstalk.

Chen WLK et al.

Abstract

A capability for analyzing complex cellular communication among tissues is important in drug discovery and development, and in vitro technologies for doing so are required for human applications. A prominent instance is communication between the gut and the liver, whereby perturbations of one tissue can influence behavior of the other. Here, we present a study on human gut-liver tissue interactions under normal and inflammatory contexts, via an integrative multi-organ platform comprising human liver (hepatocytes and Kupffer cells), and intestinal (enterocytes, goblet cells, and dendritic cells) models. Our results demonstrated long-term (>2 weeks) maintenance of intestinal (e.g., barrier integrity) and hepatic (e.g., albumin) functions in baseline interaction. Gene expression data comparing liver in interaction with gut, versus isolation, revealed modulation of bile acid metabolism. Intestinal FGF19 secretion and associated inhibition of hepatic CYP7A1 expression provided evidence of physiologically relevant gut-liver crosstalk. Moreover, significant non-linear modulation of cytokine responses was observed under inflammatory gut-liver interaction; for example, production of CXCR3 ligands (CXCL9,10,11) was synergistically enhanced. RNA-seq analysis revealed significant upregulation of IFNα/β/γ signaling during inflammatory gut-liver crosstalk, with these pathways implicated in the synergistic CXCR3 chemokine production. Exacerbated inflammatory response in gut-liver interaction also negatively affected tissue-specific functions (e.g., liver metabolism). These findings illustrate how an integrated multi-tissue platform can generate insights useful for understanding complex pathophysiological processes such as inflammatory organ crosstalk. Biotechnol. Bioeng. 2017;114: 2648-2659. textcopyright 2017 Wiley Periodicals, Inc.
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