Mitochondria are the crucial regulators for the major source of ATP for different cellular events. Due
to damage episodes, mitochondria have been established for a plethora ofalarming signals of stress that lead to
cellular deterioration, thereby causing programmed cell death. Defects in mitochondria play a key role in arbitrating
pathophysiological machinery with recent evince delineating a constructive role in mitophagy mediated mitochondrial
injury. Mitophagy has been known for the eradication of damaged mitochondria via the autophagy
process. Mitophagy has been investigated as an evolutionarily conserved mechanism for mitochondrial quality
control and homeostasis. Impaired mitophagy has been critically linked with the pathogenesis of inflammatory
diseases. Nevertheless, the exact mechanism is not quite revealed, and it is still debatable. The purpose of this
review was to investigate the possible role of mitophagy and its associated mechanism in inflammation-mediated
diseases at both the cellular and molecular levels.
In recent years, studies have begun to explore the immune involvement in head and neck tumors. Advanced stage head and neck squamous cell carcinoma (HNSCC) has a poor prognosis with low survival rates with high level of immune infiltrates. Tregs (regulatory T cells) play a crucial role in constructing an immunosuppressive tumor microenvironment. In the present study, we highlighted specific Treg markers and its factors in HNSCC solid tumors and peripheral blood of cancer patients. By histopathology and immunofluorescence staining, we observed differential expression of CD4, CD25, Foxp3, Helios and Neuropilin-1. Further, we analyzed the expression of Foxp3, Helios, Neuropilin-1 and GARP by qPCR and flow cytometry in whole blood and found to be elevated in HNSCC patients in comparison with healthy donors. Additionally, IFN-γ, TGF-β, IL-6, IL-2, IL-10 and TNF-α expressions were also found to be relatively increased in the head and neck cancer patients when compared with healthy donors. Our findings emphasize that Tregs may be involved in promoting tumor progression. Helios and Neuropilin-1 could be potent markers in identifying subsets of Tregs. Association of soluble factors could sculpture the activity of Tregs. With further research, Treg markers and its associated soluble factors could be employed to block Tregs trafficking to the tumor, thus enlightening a potential strategy for targeting human cancers.
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