Cellular reprogramming requires changes at the epigenome level that modify chromatin accessibility and enhance epigenetic plasticity. During the reprogramming process, epigenetic alterations are influenced by the induction of innate immunity, a process known as transflammation. Transflammation is mediated via toll-like receptors , which subsequently induce NF-κB. NF-κB impacts the expression of genes related to chromatin modifications. Transflammation also induces a glycolytic switch, which plays an important role in cell reprogramming and additionally prompts epigenetic modifications. When cells are reprogrammed using retroviruses, transflammation is induced by viral dsRNA through TLR3. Unlike retroviruses, the introduction of reprogramming transcription factors using non-integrative methods (e.g., mRNA, proteins), does not leave any trace at the DNA level, but is considered less efficient, possibly because the lack of transflammation. Therefor, some methods require additional stimulation of innate immunity to accelerate changes in chromatin accessibility and increase the efficiency of reprogramming. Activation of innate immunity can also induce transdifferentiation in cancerous tissues, which may result in a pro- or anti-tumor effect. The objective of this work is to review existing research on the significance of transflammation and evaluate its practical implications.
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