Human TLR2 expressing HEK293 Reporter Cells

HEK-Blue-Lucia™ hTLR2 Unit size Cat. code Docs Qty Price
Human TLR2 expressing double NF-κB–readout HEK293 reporter cells
3-7 x 10e6 cells

Notification: This cell line has been renamed. It was formerly known as "HEK-Dual™ hTLR2 (NF/IL8)". The cat. code (hkd-htlr2ni) remains unchanged.
This product is for internal research use only. Additional rights may be available. Please visit InvivoGen’s Terms and Conditions.

Human TLR2 expressing HEK293 reporter cells

Signaling pathways in HEK-Blue-Lucia™ hTLR2 cells
Signaling pathways in HEK-Blue-Lucia™ hTLR2 cells

InvivoGen offers a human embryonic kidney 293 (HEK293)-derived cell line, specifically designed to assess the distinct role of the human Toll-like receptor 2 (hTLR2):

— HEK-Blue-Lucia™ hTLR2 cells* 

These cells were generated from the HEK-Blue-Lucia™ Null​ cell line harboring two inducible reporter genes. This feature allows the double readout of the NF-κB/AP-1 pathway, by monitoring the SEAP (secreted embryonic alkaline phosphatase) or Lucia luciferase activities. HEK-Blue-Lucia™ hTLR2 cells also stably express the hTLR2 and CD14 genes. Due to a triple knockout (KO) of TLR3, TLR5, and TNFR, this cell line allows for the independent study of TLR2.


Stimulation of HEK-Blue-Lucia™ hTLR2 cells with TLR2 agonists (e.g. Pam3CSK4) triggers the activation of the artificial NF-κB-inducible promoter and the subsequent production of SEAP. It also promotes the expression of Lucia luciferase, which is knocked in (KI) downstream of the endogenous (more physiological) IL-8 promoter (see figures).

IL-8 (interleukin 8) is a chemokine produced in response to TLR agonists in an NF-κB/AP-1-dependent manner [1-2]. This feature enables the double readout study of the NF-κB/AP-1 pathway, by monitoring the activity of SEAP and Lucia luciferase using QUANTI-Blue™ Solution (SEAP detection reagent) or QUANTI-Luc™ 4 Lucia/Gaussia (luciferase detection reagent), respectively. Thus, you may choose the readout depending on your laboratory equipment utilizing a spectrophotometer for SEAP or a luminometer for Lucia luciferase detection.

TLR2 is an important pattern recognition receptor (PRR) detecting a large spectrum of microbial pathogen-associated molecular patterns (PAMPs) from Gram-positive and Gram-negative bacteria as well as fungi, parasites, and viruses [3].

More details More details


Read our review Read our review on TLR2


Key features:

  • Stable overexpression of hTLR2 and CD14
  • Verified KO for the TLR3, TLR5, and TNFR genes 
  • Functionally validated using a selection of PRR ligands and cytokines
  • Readily assessable NF-κB activation by assessing the SEAP and/or Lucia luciferase activities


  • Defining the role of TLR2-dependent NF-κB signaling pathway
  • Screening for novel TLR2 agonists and inhibitors
  • Choice of readout depending on the laboratory equipment (spectrophotometer for SEAP or luminometer for Lucia luciferase detection).


* formerly named HEK-Dual™ hTLR2 (NF/IL8) cells



1. Roebuck KA. 1999. Regulation of interleukin-8 gene expression. J Interferon Cytokine Res:429-38.
2. Ohta K, et al. 2014. Toll-like receptor (TLR) expression and TLR‑mediated interleukin-8 production by human submandibular gland epithelial cells. Mol Med Rep. (5):2377-82.
3. Oliveira-Nascimento, L. et al. 2012. The Role of TLR2 in Infection and Immunity. Front Immunol 3, 79.


NF-κB - SEAP response
NF-κB - SEAP response

NF-κB–SEAP response. HEK-Blue-Lucia™ hTLR2  and HEK-Blue™ hTLR2 cells were stimulated with various TLR agonists: FSL-1 (TLR2 agonist; 30 pg/ml), Pam3CSK4 (TLR2 agonist; 30 pg/ml), HKLM (TLR2 agonist; 1x107 cells/ml), Poly(I:C) (TLR3 agonist; 3 µg/ml), FLA-ST (flagellin from S. typhimurium, TLR5 agonist; 100 ng/ml), and TNF-α (10 ng/ml). After overnight incubation, the activation of NF-κB was assessed by measuring the activity of SEAP in the supernatant using QUANTI-Blue™ Solution. Data are shown as optical density (OD) at 655 nm (mean ± SEM).

NF-κB (IL-8) - Lucia response
NF-κB (IL-8) - Lucia response

NF-κB (IL-8)–Lucia response using QUANTI-Luc™. HEK-Blue-Lucia™ hTLR2 cells were stimulated with TLR2 agonists: FSL-1 (TLR2 agonist; 30 pg/ml), Pam3CSK4 (TLR2 agonist; 30 pg/ml) and HKLM (1x107 cells/ml). After 24h incubation, activation of the IL-8 was assessed by measuring the activity of Lucia luciferase in the supernatant using QUANTI-Luc™. Data are shown in fold response over non-induced cells (mean ± SEM).

Back to the top


Antibiotic resistance: BlasticidinHygromycinZeocin®

Growth medium: DMEM, 4.5 g/l glucose, 2 mM L-glutamine, 10% (v/v) heat-inactivated fetal bovine serum, 100 U/ml penicillin, 100 μg/ml streptomycin, 100 μg/ml Normocin™

Quality Control:

  • Human TLR2 and CD14 overexpression has been verified by flow cytometry and functional assays.
  • The triple KO of TLR3, TLR5, and TNFR has been verified by DNA sequencing, PCR, and functional assays.
  • The stability for 20 passages, following thawing, has been verified.
  • These cells are guaranteed mycoplasma-free. 

Note: HEK-Blue-Lucia™ hTLR2 cells are resistant to BlasticidinHygromycin, and Zeocin®. They should be maintained in growth medium supplemented with Hygromycin and Zeocin®.


These cells are covered by a Limited Use License (See Terms and Conditions).

Back to the top


Dry Ice Shipped on dry ice (Europe, USA, Canada, and some areas in Asia)

Back to the top


Toll-like receptor 2 (TLR2) plays an essential role in detecting a diverse range of microbial pathogen-associated molecular patterns (PAMPs) from Gram-positive and Gram-negative bacteria as well as fungi, parasites, and viruses. These PAMPs include cell-wall components such as lipoproteins, lipoteichoic acid (LTA; Gram-positive bacteria only), lipoarabinomannan (mycobacteria only), and zymosan (yeast) [1]. TLR2 forms a heterodimer on the cell surface, crucial for signaling and ligand specificity, with co-receptors TLR1 or TLR6. For example, TLR2-TLR1 and TLR2-TLR6 heterodimers are known to bind specific lipoproteins depending on whether they are tri- or diacylated, respectively [2, 3]. Moreover, ligand recognition is enhanced by its non-specific delivery to TLR2 by CD14, and sometimes in combination with additional ligand-specific molecules such as CD36 and Dectin-1 [4, 5].

Upon ligand recognition, TLR2-dependent signaling cascades ultimately lead to a MyD88 and MAL/TIRAP-dependent activation of pro-inflammatory transcription factors such as NF-κB and AP-1 [6]. Additionally, the PI3K/Akt pathway may also be activated leading to the production of anti-inflammatory cytokines [7]. Interestingly, microarray data generated by InvivoGen clearly highlights that downstream effects differ depending on whether it’s the TLR2-TLR1 or TLR2-TLR6 heterodimer that is activated upon ligand recognition.



1. Oliveira-Nascimento, L. et al. 2012. The Role of TLR2 in Infection and Immunity. Front Immunol 3, 79.
2. Takeuchi, O. et al. 2001. Discrimination of bacterial lipoproteins by Toll-like receptor 6. Int Immunol 13, 933-940.
3. Takeuchi, O. et al. 2002. Cutting edge: role of Toll-like receptor 1 in mediating immune response to microbial lipoproteins. J Immunol 169, 10-14.
4. Jimenez-Dalmaroni, M.J. et al. 2009. Soluble CD36 ectodomain binds negatively charged diacylglycerol ligands and acts as a co-receptor for TLR2. PLoS One 4, e7411.
5. Lotz, S. et al. 2004. Highly purified lipoteichoic acid activates neutrophil granulocytes and delays their spontaneous apoptosis via CD14 and TLR2. J Leukoc Biol 75, 467-477.
6. Piao, W. et al. 2016. Differential adapter recruitment by TLR2 co-receptors. Pathog Dis 74.
7. Santos-Sierra, S. et al. 2009. Mal connects TLR2 to PI3Kinase activation and phagocyte polarization. EMBO J 28, 2018-2027.

Back to the top

FAQ Cell Lines

Visit our FAQ Any questions about our cell lines ? Visit our frequently asked questions page

Back to the top


Customer Service
& Technical Support
Shopping cart is empty