Reliably isolate mononuclear cells from peripheral blood, cord blood, or bone marrow with Lymphoprep™—a cost-effective alternative to Ficoll-Paque™. Use this density gradient medium for rapid, simple, and reliable cell isolation from most blood samples obtained from normal individuals and patients. You can substitute Lymphoprep™ for Ficoll-Paque™ without changing your existing protocols and achieve similar cell purity and recovery rates. This medium is fully compatible with both SepMate™ and RosetteSep™. Formulated with sodium diatrizoate (9.1% w/v) and polysaccharide (5.7% w/v), Lymphoprep™ has a density of 1.077 g/ml.
Data Figures
Figure 1. Purity and Recovery of Cells from Whole Blood When Using Cost-Effective Lymphoprep™ is Comparable to Using Ficoll-Paque™ PLUS
(A) Density gradient centrifugation of peripheral whole blood using Lymphoprep™ results in similar cell purity of mononuclear cells including T cells, B cells, NK cells and monocytes compared to Ficoll-Paque™ PLUS. (B) The recovery of total mononuclear cells and CD45+ cells is also similar. (n = 5, Mean ± SD).
Figure 2. Purity and Recovery of Cells from Cord Blood When Using Cost-Effective Lymphoprep™ is Comparable to Using Ficoll-Paque™ PLUS
(A) Density Gradient centrifugation of cord blood using Lymphoprep™ results in similar cell purity of mononuclear cells including T cells, B cells, NK cells and monocytes compared to Ficoll-Paque™ PLUS. (B) The recovery of total mononuclear cells and CD45+ cells is also similar. (n = 4, Mean ± SD).
This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.
Chemoproteomic development of SLC15A4 inhibitors with anti-inflammatory activity. T.-Y. Chiu et al. Nature chemical biology 2024 aug
Abstract
SLC15A4 is an endolysosome-resident transporter linked with autoinflammation and autoimmunity. Specifically, SLC15A4 is critical for Toll-like receptors (TLRs) 7-9 as well as nucleotide-binding oligomerization domain-containing protein (NOD) signaling in several immune cell subsets. Notably, SLC15A4 is essential for the development of systemic lupus erythematosus in murine models and is associated with autoimmune conditions in humans. Despite its therapeutic potential, the availability of quality chemical probes targeting SLC15A4 functions is limited. In this study, we used an integrated chemical proteomics approach to develop a suite of chemical tools, including first-in-class functional inhibitors, for SLC15A4. We demonstrate that these inhibitors suppress SLC15A4-mediated endolysosomal TLR and NOD functions in a variety of human and mouse immune cells; we provide evidence of their ability to suppress inflammation in vivo and in clinical settings; and we provide insights into their mechanism of action. Our findings establish SLC15A4 as a druggable target for the treatment of autoimmune and autoinflammatory conditions.
NETosis and thrombosis in vaccine-induced immune thrombotic thrombocytopenia. H. H. L. Leung et al. Nature communications 2022 sep
Abstract
Vaccine-induced immune thrombotic thrombocytopenia (VITT) is a rare yet serious adverse effect of the adenoviral vector vaccines ChAdOx1 nCoV-19 (AstraZeneca) and Ad26.COV2.S (Janssen) against COVID-19. The mechanisms involved in clot formation and thrombocytopenia in VITT are yet to be fully determined. Here we show neutrophils undergoing NETosis and confirm expression markers of NETs in VITT patients. VITT antibodies directly stimulate neutrophils to release NETs and induce thrombus formation containing abundant platelets, neutrophils, fibrin, extracellular DNA and citrullinated histone H3 in a flow microfluidics system and in vivo. Inhibition of NETosis prevents VITT-induced thrombosis in mice but not thrombocytopenia. In contrast, in vivo blockage of Fc$\gamma$RIIa abrogates both thrombosis and thrombocytopenia suggesting these are distinct processes. Our findings indicate that anti-PF4 antibodies activate blood cells via Fc$\gamma$RIIa and are responsible for thrombosis and thrombocytopenia in VITT. Future development of NETosis and Fc$\gamma$RIIa inhibitors are needed to treat VITT and similar immune thrombotic thrombocytopenia conditions more effectively, leading to better patient outcomes.
IL-6 drives T cell death to participate in lymphopenia in COVID-19. X. Zhou et al. International immunopharmacology 2022 oct
Abstract
Lymphopenia is a common observation in patients with COVID-19. To explore the cause of T cell lymphopenia in the disease, laboratory results of 64 hospitalized COVID-19 patients were retrospectively analyzed and six patients were randomly selected to trace their changes of T lymphocytes and plasma concentration of IL-6 for the course of disease. Results confirmed that the T-cell lymphopenia, especially CD4+ T cell reduction in COVID-19 patients, was a reliable indicator of severity and hospitalization in infected patients. And CD4+ T cell count below 200 cells/$\mu$L predicts critical illness in COVID-19 patients. In vitro assay supported that exposure to key contributors (IL-1$\beta$, IL-6, TNF-$\alpha$ and IFN-$\gamma$) of COVID-19 cytokine storm caused substantial death of activated T cells. Among these contributors, IL-6 level was found to probably reversely correlate with T cell counts in patients. And IL-6 alone was potent to induce T cell reduction by gasderminE-mediated pyroptosis, inferring IL-6 took a part in affecting the function and status of T cells in COVID-19 patients. Intervention of IL-6 mediated T cell pryprotosis may effectively delay disease progression, maintain normal immune status at an early stage of infection.
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