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Abstract
Immunotherapy options for patients with cancer have emerged following decades of research on immune responses against tumors. Most treatments in this category harness T cells with specificity for tumor associated antigens, neoantigens, and cancer-testis antigens. GSK3β is a serine-threonine kinase with the highest number of substrates and multifaceted roles in cell function including immune cells. Importantly, inhibitors of GSK3β are available for clinical and research use. Here, we review the possible role of GSK3β in the immune tumor microenvironment, with goal to guide future research that tests GSK3β inhibition as an immunotherapy adjunct.
Highlights
It is a truism that non-synonymous mutations bear the potential to generate neoantigens and elicit immune reactions against tumors [1]
A growing body of literature supports a multifaceted role for Glycogen Synthase Kinase 3β (GSK3β) in the immune tumor microenvironment
This is not a surprise as GSK3β is the busiest kinase in the cell based on the number of known and predicted substrates, many of which are key regulators of the immune response to tumors
Summary
It is a truism that non-synonymous mutations bear the potential to generate neoantigens and elicit immune reactions against tumors [1]. The main lymphocyte populations include either CD4 or CD8 positive cells. CD4 positive, or “helper” T lymphocytes (Th) further divide into Th1, Th2, and Th17 subgroups under the influence of cytokine and chemokine cues [10] Their main role is to prime B lymphocyte activation [11, 12] and antigen presentation to CD8+ cells [13] whereas they can. GSK3β in Tumor Immune Microenvironment function as cytotoxic T lymphocytes (CTLs) [14]. In “hot” tumors, immune check points like the PD1-PDL1 axis play a central role in immune evasion This system is highly regulated by interplay between cancer related mutations, the cytokine and chemokine milieu and importantly activation of molecular pathways in the adaptive immune system cells.
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