Regulatory T-cell (Treg) suppression & the IL-2 axis
Regulatory T-cell (Treg) suppression & the IL-2 axis. Tregs restrain anti-tumour immunity. High-affinity CD25 (IL-2Rα) drives a JAK–STAT5→FOXP3 programme and lets Tregs act as an IL-2 sink, while CTLA-4 strips co-stimulation and IL-10 / TGF-β dampen effector T cells. Click any protein for the matching Assay Genie In Vivo functional-grade antibody (surface / cytokine targets) or ELISA kit (signalling proteins).
Regulatory T cells (Tregs) enforce peripheral tolerance and are enriched in tumours, where they blunt anti-tumour responses. Their identity depends on the transcription factor FOXP3, induced and sustained by IL-2 signalling: IL-2 binds the high-affinity receptor (CD25 / IL-2Rα plus CD122 and γc), activating JAK1 / JAK3 and STAT5, which — together with TCR-driven NFAT — drives FOXP3 and reinforces CD25 and CTLA-4.
Tregs suppress effector T cells through several routes: as an IL-2 sink (their high-affinity CD25 out-competes effectors for IL-2), by CTLA-4 trans-endocytosis of CD80/86 from dendritic cells (removing co-stimulation), and by secreting the inhibitory cytokines IL-10 and TGF-β. The net effect is reduced effector proliferation and cytokine output.
Assay Genie In Vivo functional-grade antibodies target this axis two ways: depletion (anti-CD25, anti-CTLA-4) and suppression blockade (anti-IL-2 / IL-2 complexes, anti-IL-10, anti-TGF-β, anti-CD127), both used to relieve Treg-mediated immunosuppression in vivo. For research use only; not for diagnostic or therapeutic procedures. Mouse targets shown.
Every protein node links to a product: surface / cytokine targets open Assay Genie In Vivo antibodies; signalling proteins open the matching ELISA kit.