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In women with endometriosis, Toll-like receptor 4 (TLR4) is upregulated in macrophages and endometrial stromal cells, where stimulation with heat-shock protein 70 or lipopolysaccharide (LPS) enhances secretion of proinflammatory cytokines such as IL-6 and TNF-α, and promotes stromal cell proliferation effects that can be blocked by TLR4 inhibition (Khan et al., 2008)
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