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The relationship between innate and adaptive immunity underscores their value: innate triggers, such as DAMPs from stressed melanocytes, may initiate adaptive responses via antigen presentation, creating a self-amplifying loop

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By integrating transcriptomic and untargeted metabolomic analyses of BM neutrophils, we revealed a pivotal role for Chac2-driven GSH metabolic reprogramming in skewing neutrophils toward the N1 phenotype, which is orchestrated by upstream IFN-I signaling

curcumin, which helps maintain genomic stability and modulates telomere-associated proteins