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

Figure 2. β2M induced monocyte inflammatory responses.

Figure 2

(A) THP-1 cells were treated with β2M, and IL-8 release was determined by ELISA. β2M induced inflammatory molecule production in a time- and dose-dependent manner (n = 4, *P < 0.05, **P < 0.01 vs. 0, 1-way ANOVA with Bonferroni correction). (B and C) β2M induced a primary mouse monocyte proinflammatory phenotype. Mouse BM monocytes were isolated and treated with control PBS or β2M (5 μg/ml). (B) Forty-eight hours later, Ly6C surface expression was measured by flow cytometry (n = 9, control; n = 8, β2M; **P < 0.01, unpaired 2-tailed t test with Welch’s correction). (C) KC and IL-6 release determined by ELISA (n = 9, control; n = 8, β2M; **P < 0.01, unpaired 2-tailed t test with Welch’s correction). (D) β2M induced a human monocyte inflammatory phenotype. Human peripheral blood monocytes were isolated and treated with control PBS or β2M (10 μg/ml). CD16 surface expression was measured by flow cytometry (right panel, n = 4, *P < 0.05, unpaired 2-tailed t test with Welch’s correction) and IL-8 release by ELISA (left panel, n = 4 control, n = 7 β2M, *P < 0.05, unpaired 2-tailed t test with Welch’s correction). All graphs represent experiments that were repeated at least twice.