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. 2019 Mar 7;4(5):e122943. doi: 10.1172/jci.insight.122943

Figure 4. β2M proinflammatory phenotype signaling is through noncanonical TGFβ receptor signaling.

Figure 4

(A) Inhibition of TGFβR signaling ameliorated β2M-induced monocyte activation. Mouse monocytes were incubated with control buffer, β2M, or β2M and a TGFβR1 kinase inhibitor (SB431542). KC production was determined 48 hours later (n = 4; **P < 0.01, 1-way ANOVA with Bonferroni correction). (B) β2M binds to TGFβR1 and TGFβR2. Fc-TGFβR1 or Fc-TGFβR2 were immobilized on a sensor chip, and β2M, TGFβ1, or TGFβ3 binding was determined by SPR. (C and D) WT and TGFβR2–/– monocytes were incubated with control buffer or β2M. (C) β2M induced WT, but not TGFβR–/– monocyte, Ly6Chi phenotype. (D) Quantification of C (n = 4; *P < 0.05, 1-way ANOVA with Bonferroni correction).