ioMicroglia TREM2 R47H/WT are opti-ox™ precision reprogrammed microglia carrying a genetically engineered heterozygous R47H mutation in the TREM2 gene encoding the triggering receptor expressed on myeloid cells 2 protein. The TREM2 R47H mutation has been linked with increased risk of late-onset Alzheimer's disease (AD).
These cells offer a functional, rapidly maturing, and disease relevant system to study the role of the TREM2 R47H mutation in late-onset AD, alongside a genetically matched wild-type control.
Related disease model cells are available with a homozygous TREM2 R47H mutation, and both can be used alongside their genetically matched control, ioMicroglia™. The disease model cells and the wild-type control offer a physiologically relevant model to investigate the impact of the TREM2 R47H mutation on cellular and molecular mechanisms and function in late-onset AD.
Place your order
Confidently investigate your phenotype of interest across multiple clones with our disease model clone panel. Detailed characterisation data (below) and bulk RNA sequencing data (upon request) help you select specific clones if required.
A maximum number of 20 vials applies. If you would like to order more than 20 vials, please contact us at firstname.lastname@example.org.
ioMicroglia TREM2 R47H/WT are delivered in a cryopreserved format and are programmed to rapidly mature upon revival in the recommended media. The protocol for the generation of these cells is a three-phase process: an Induction phase that is carried out at bit.bio, Phase 1: Stabilisation for 24 hours, Phase 2: Maturation for a further 9 days, Phase 3: the Maintenance phase. Cells are ready to use from day 10.
Highly characterised and defined
Disease model cells express key microglia markers comparably to the genetically matched wild-type control
Immunofluorescent staining on day 10 post-revival demonstrates similar homogenous expression of microglia markers P2RY12 and IBA1 and ramified morphology in the disease model clone compared to the genetically matched wild-type (WT) control. 100X magnification.
Disease model cells show expected ramified morphology by day 10
The disease model clone matures rapidly and key ramified morphology can be identified by day 4 and continues through to day 10, similarly to the WT control. Day 1 to 10 post-thawing; 100x magnification.
Key phagocytic function
Disease model cells show a reduced proportion of phagocytosis ofE.coliparticles compared to the genetically matched wild-type control
Phagocytosis was analysed at day 10 post-revival after incubation with 1 µg/0.33 cm2 pHrodo™ RED labelled E. coli particles for 24 hours +/- cytochalasin D control. The graph displays the proportion of cells phagocytosing E. coli particles over 24 hours and shows that the disease model clone displays a reduced proportion of phagocytosis than the WT control. Images were acquired every 30 mins on the Incucyte® looking at red fluorescence and phase contrast. Three technical replicates were performed per experiment.
Disease model cells show a reduced degree of phagocytosis ofE. coliparticles compared to the genetically matched wild-type control
Phagocytosis was analysed at day 10 post-revival after incubation with 1 µg/0.33 cm2 pHrodo™ RED labelled E. coli particles for 24 hours +/- cytochalasin D control. The graph displays the fluorescence intensity per cell displaying degree of phagocytosis per cell and shows that the disease model clone displays a reduced degree of phagocytosis per cell than the WT control. Images were acquired every 30 mins on the Incucyte® looking at red fluorescence and phase contrast. Three technical replicates were performed per experiment.
Key cytokine secretion function
Disease model cells display reduced secretion of pro-inflammatory cytokines upon activation compared to the genetically matched wild-type control
Cytokine secretion was analysed at day 10 post-revival after stimulation with LPS 100 ng/ml and IFNɣ 20 ng/ml for 24 hours. This revealed that the disease model clone secretes the predominantly pro-inflammatory cytokines, IL-6, IL-8, IL-10, IL-12p70, IL-1β, and TNF⍺ at a lower level than the WT control. Supernatants were harvested and analysed using MSD V-plex Proinflammatory Kit™. Three technical replicates were performed per experiment.
Human iPSC line
6, 12, 24, 96 & 384 well plates
Caucasian adult male (skin fibroblast)
Small: >1.5 x 10⁶ viable cells
Sterility, protein expression (ICC), functional phagocytosis and cytokine secretion assays
opti-ox cellular reprogramming
Recommended seeding density
37,000 to 39,500 cells/cm²
LN2 or -150°C
ioCells are for research use only
Heterozygous R47H mutation in the TREM2 gene
Alzheimer's disease modelling Drug discovery and development Neuroinflammation modelling Phagocytosis assays Cytokine response assays Co-culture studies
Alzheimer’s Disease Pathogenesis - Emerging Role of Microglia
In this GEN webinar, hear from our distinguished expert, Dr Matthias Pawlowski, and learn about the emerging role of microglia in the pathogenesis of Alzheimer’s disease and their potential as a therapeutic target to treat this disease effectively.