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Start with ready-to-use, ethically sourced, primary human macrophages. With personalized service, custom products, flexible delivery times, and the option to reserve entire lots to prescreen cells for applications, we help you get the cells you need.
Immunomagnetically selected peripheral blood monocytes are cultured in RPMI 1640 Medium (Catalog #36750) + 10% FBS, M-CSF, and IL-4 for 5 days to generate macrophages. IL-4 in combination with M-CSF may induce M2a-like properties. Cells are collected using Institutional Review Board (IRB)-approved consent forms and protocols and cryopreserved in animal component-free CryoStor®CS10 medium (Catalog #07930). Additional documentation and high-resolution HLA typing (Class I and Class II alleles and CMV status) are available upon request. Acid-citrate-dextrose solution A (ACDA) is added during collection as an anticoagulant. Donor specifications (e.g. BMI category, smoking status, ethnicity, etc.) can be requested in the comment box above. Donors are screened for HIV-1, HIV-2, hepatitis B, and hepatitis C.
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This product is designed for use in the following research area(s) as part
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TMEM173 Drives Lethal Coagulation in Sepsis.
H. Zhang et al.
Cell host {\&} microbe 2020
Abstract
The discovery of TMEM173/STING-dependent innate immunity has recently provided guidance for the prevention and management of inflammatory disorders. Here, we show that myeloid TMEM173 occupies an essential role in regulating coagulation in bacterial infections through a mechanism independent of type I interferon response. Mechanistically, TMEM173 binding to ITPR1 controls calcium release from the endoplasmic reticulum in macrophages and monocytes. The TMEM173-dependent increase in cytosolic calcium drives Gasdermin D (GSDMD) cleavage and activation, which triggers the release of F3, the key initiator of blood coagulation. Genetic or pharmacological inhibition of the TMEM173-GSDMD-F3 pathway blocks systemic coagulation and improves animal survival in three models of sepsis (cecal ligation and puncture or bacteremia with Escherichia coli or Streptococcus pneumoniae infection). The upregulation of the TMEM173 pathway correlates with the severity of disseminated intravascular coagulation and mortality in patients with sepsis. Thus, TMEM173 is a key regulator of blood clotting during lethal bacterial infections.
Design of a novel integration-deficient lentivector technology that incorporates genetic and posttranslational elements to target human dendritic cells.
Tareen SU et al.
Molecular therapy : the journal of the American Society of Gene Therapy 2014 MAR
Abstract
As sentinels of the immune system, dendritic cells (DCs) play an essential role in regulating cellular immune responses. One of the main challenges of developing DC-targeted therapies includes the delivery of antigen to DCs in order to promote the activation of antigen-specific effector CD8 T cells. With the goal of creating antigen-directed immunotherapeutics that can be safely administered directly to patients, Immune Design has developed a platform of novel integration-deficient lentiviral vectors that target and deliver antigen-encoding nucleic acids to human DCs. This platform, termed ID-VP02, utilizes a novel genetic variant of a Sindbis virus envelope glycoprotein with posttranslational carbohydrate modifications in combination with Vpx, a SIVmac viral accessory protein, to achieve efficient targeting and transduction of human DCs. In addition, ID-VP02 incorporates safety features in its design that include two redundant mechanisms to render ID-VP02 integration-deficient. Here, we describe the characteristics that allow ID-VP02 to specifically transduce human DCs, and the advances that ID-VP02 brings to conventional third-generation lentiviral vector design as well as demonstrate upstream production yields that will enable manufacturing feasibility studies to be conducted.
