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As a result, almost every PRR has been implicated in progression of ALD (6, 60) (Figure 2), including intracellular receptors such as TLR3/7/8/9, cGAS, AIM2, NLRs, and extracellular receptors such as TLR2/4 and the C-type lectin receptors (CLRs)

Our analyses allowed us to establish a parallelism around the bi-directional interactions between host and bacteria, ultimately informing on the possible cause-effect relationship behind the observed phenotype

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