Next, we observed that the MyD88 −/− mice were completely protected from renal dysfunction caused by sepsis, while the TLR2 −/− and TLR4 −/− animals only seemed to improve but did not reach statistical significance ( Figure 1c and 1d ).
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TLR2, TLR4 and the MYD88 signaling pathway are crucial for neutrophil migration in acute kidney injury induced by sepsis.
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