Abstract
Along with the clinical success of immuno-oncology drugs and cellular therapies, T-cell biology has attracted considerable attention in the immunology community. Long-term immunity, traditionally analyzed in the context of infection, is increasingly studied in cancer. Many signaling pathways, transcription factors, and metabolic regulators have been shown to participate in the formation of memory T cells. There is increasing evidence that the signal transducer and activator of transcription-3 (STAT3) signaling pathway is crucial for the formation of long-term T-cell immunity capable of efficient recall responses. In this review, we summarize what is currently known about STAT3 role in the context of memory T-cell formation and antitumor immunity.
Highlights
Along with the clinical success of immuno-oncology drugs and cellular therapies, T-cell biology has attracted considerable attention in the immunology community
The connection between tumor progression and signal transducer and activator of transcription-3 (STAT3) driven metabolism was discovered [99]. They showed that in a spontaneous breast cancer model, ablating leptin-driven STAT3 signaling in CD8+ T cells enhanced the antitumor effect by reducing fatty acid oxidation (FAO) and promoting glycolysis
There is a need for cleaner models that interrogate STAT3 in mature T cells
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. STAT3 binds to phosphor(p)YXXQ motifs on the receptor and is subsequently phosphorylated at Tyr705 by JAK [5,6] This modification allows STAT3 to dimerize and initiate transcription regulation [7]. More importantly for the T-cell context, STAT3 signaling is required for hematopoiesis [36–38] and the proper development of the thymus [39–41] and can lead to abnormalities if perturbed. There is increasing evidence that STAT3 signaling plays a role at the late stage of T-cell development [42,43]. Tfh (follicular helper) subset subset is characterized by CXCR5 expression isand necessary for B-cell activation and germinal center formation [49]. BCL-6 is theislineageis necessary for B-cell activation and germinal center formation It is eage-defining factor of Tfh, whose expression is positively regulated[48,50]. It is important to note that, in these settings, lineage-defining factors such as differentiation into specific CD4+. Tion is driven by the STAT4–T-bet signaling axis and suppresses alternative CD4+ T-cell fates [54]
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