Committed to providing comprehensive support for global drug development

Dectins (dendritic cell-associated C-type lectins)—particularly Dectin-1—constitute a critical class of pattern recognition receptors (PRRs) within the immune system, belonging to the C-type lectin receptor (CLR) family. As a key type II transmembrane protein, Dectin-1 was the first non-TLR pattern recognition receptor discovered to possess intracellular signaling capabilities; it is primarily expressed on the surface of myeloid immune cells, such as macrophages, neutrophils, and dendritic cells. Through its extracellular domain, Dectin-1 specifically recognizes the unique β-glucans (specifically β-1,3 and β-1,6 glucans) found within fungal cell walls, thereby mediating the binding, phagocytosis, and killing of fungi by immune cells, while simultaneously inducing the production of cytokines and chemokines to initiate an inflammatory response. Beyond its antifungal functions, recent studies have revealed that Dectin-1 plays a complex and pivotal role in the recognition of mycobacteria, the regulation of autoimmune diseases (such as inflammatory bowel disease and type 1 diabetes), and cancer immunosurveillance.

Upon recognition of the insoluble β-glucans in fungal cell walls by its extracellular domain, Dectin-1 undergoes receptor clustering, leading to the phosphorylation of its intracellular ITAM motifs; this event directly recruits and activates Spleen Tyrosine Kinase (Syk). The activated Syk subsequently triggers either the NF-κB or the Raf-1 signaling pathway. These two pathways act synergistically to induce the production of inflammatory factors (e.g., TNF-α, IL-6), chemokines, and cytokines associated with Th17 polarization (e.g., IL-23, IL-1β), thereby bridging the gap between innate and adaptive immunity—specifically, the Th17 cell response.

The HEK293 Human Dectin1a Effector Reporter Cell(Adherent)  model effectively simulates the in vivo Dectin1a signal transduction process, the principle is illustrated in the figure below.

Figure 1. Schematic diagram of the HEK293 Human Dectin1a Effector Reporter Cell(Adherent) model

Figure 2. Recombinant Dectin1a Effector Reporter Cell(Adherent) stably expressing Dectin1a.



Figure 3. Dose Response of Ligands in Dectin-1a Effector Reporter Cell( Adherent, C49).

Cell Resuscitation
1)Rapidly thaw the frozen cells in a 37 °C water bath for approximately 60 seconds. Once thawed (which may take slightly less or more than 60 seconds), immediately transfer the cell suspension from the cryovial into a 15 mL centrifuge tube containing 10 mL of pre-warmed HEK293 Human Dectin1a Effector Reporter Cell(Adherent) complete culture medium.
2)Centrifuge cells at 1000 rpm for 5 min to remove medium, then resuspend cells in 5 mL of pre-warmed complete medium.
3)Transfer the cell suspension into a T25 culture flask and incubate at 37 °C with 5% CO₂.
4)After approximately 24–36 hours, replace the medium or passage the cells to remove non-adherent dead cells.

Subculturing procedure
1)When the cell density reaches the appropriate confluency for passaging, wash the cells with PBS, then add 1 mL trypsin to detach the cells. When more than 80% of the cells detach upon gently tapping the culture flask, add complete culture medium to terminate digestion. Gently pipette to obtain a single-cell suspension, transfer to a 15 mL centrifuge tube, and centrifuge at 1000 rpm for 5 minutes.

2)Discard supernatant after centrifugation. Resuspend cells in fresh medium to a single-cell suspension and transfer to a new culture flask for continued growth.

Cell Freezing
After trypsinization and centrifugation of cells from each T75 flask or 10 cm culture dish, discard the supernatant. Add 2 mL of cryopreservation medium (90% FBS + 10% DMSO), gently resuspend thoroughly, and aliquot into two cryovials. Immediately place the cryovials into a controlled-rate freezing container (e.g., Nalgene 5100-0001), fill with isopropanol to the indicated level, and store at −80 °C. After 24 hours, transfer the cryovials to liquid nitrogen for long-term storage.