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Within a tumor microenvironment, immunosuppressive Tregs can prevent T effector cells from properly detecting and destroying tumor antigens. Liu et al. began to investigate the mechanism Tregs are using for this suppression, finding indications that the Tregs became a sink for glucose and the resulting withdrawal caused effector/naive T cells to become senescent. The loss of glucose triggered an ATM-associated DNA damage response. They also found that MAPK, ERK1/2, p38, and STAT1/STAT3 signaling led to increased expression of p53, p21, and p16, which arrested the cell cycle and caused senescence. These studies help to define human Treg mechanisms of suppression and have important implications in immunotherapies and cancer treatments.

BioLegend provides several sensitive antibodies for the detection of phosphorylated proteins involved in these signaling pathways along with True-Phos™ Perm Buffer, which is specially designed for the detection of phosphorylated protein targets in intracellular flow cytometry staining.
Adapted from Liu, X. et al. 2018. Nat. Commun. 9:249. Pubmed
Specificity Clone
BTK Phospho (Tyr223) A16128B
BTK Phospho (Tyr223)/ITK Phospho (Tyr180) A16128C
BTK Phospho (Tyr551)/ITK Phospho (Tyr512) A16064A
ERK1/2 Phospho (Thr202/Tyr204) 6B8B69
p38 MAPK Phospho (Thr180/Tyr182) Poly29035
STAT3 Phospho (Tyr705) 13A3-1
STAT3 Phospho (Ser727) A16089B
STAT6 Phospho (Tyr641) A15137A
Related Products
True-Phos™ Perm Buffer Chk2 p38 MAPK
Western-Ready™ ECL Substrate Kit H2A.X Phospho
(Ser139) 		p53
Direct-Blot™ HRP Conjugated Antibodies p16 (CDKN2A) STAT1
ATM Phospho (Ser1981) p21 (CDKN1A) STAT3
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