Fig. 9: The mechanism by which TMPRSS11E regulates the macrophage IFN-γ-STAT1 response pathway by cleaving surface TFR1 during inflammation. | Communications Biology

Fig. 9: The mechanism by which TMPRSS11E regulates the macrophage IFN-γ-STAT1 response pathway by cleaving surface TFR1 during inflammation.

From: TMPRSS11E-mediated TFR1 cleavage influences IFN-γR2 internalization and the macrophage innate response

Fig. 9

In macrophages, LPS induced the expression of TMPRSS11E, which then cleaved the cell-surface transferrin receptor TFR1, releasing sTFR1. The increased sTFR1 may be a marker of inflammatory status. The cleavage of TFR1 by TMPRSS11E affects iron uptake and the internalization of IFN-γR2. The increased presence of IFN-γR2 on the cell membrane sensitizes IFN-γ signaling and promotes the macrophage pro-inflammatory M1 polarization. DMT1 divalent metal transporter 1, STEAP six-transmembrane epithelial antigen of prostate.

Back to article page