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Endogenous danger signals secreted from cells under pathological stimuli, including cell-free DNA, modulate intracellular proinflammatory signaling in an autocrine/paracrine manner through TLRs on the cell surface [15]

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Data from the CT-infected, hormone-naive (CTN) group establish that CT is the primary driver of damage, whereas the hormonal milieu, particularly progesterone, acts as a potent modulator, either exacerbating or mitigating the pathological cascade