p(HGNC:CD86)
Similarly, NAC prevented increased expression of MHCII, CD14, TNFα, IL-6, IL-1β, and CD86 and mildly compensated for the decrease of CD206 and IL-10 following heme treatment (Figure 4D; supplemental Figure 5). PubMed:26675351
Likewise, heme and FeNTA treatment causes the induction of the M1 markers MHCII, CD86, CD14, TNFα, IL-6, and IL1β and a decrease in the M2 markers CD206, IL-10, and Arginase-1 (the last with FeNTA only) in M0 BMDMs (Figure 3A; supplemental Figures 5, 6A, and 7). PubMed:26675351
Importantly, 15 hours after heme injection, hepatic macrophages showed iron deposition (data not shown) and an increased expression of the M1 markers MHCII and CD86 and reduced levels of the M2 markers CD206 and Arginase-1 compared with nontreated mice. PubMed:26675351
Likewise, splenic macrophages from heme-treated mice show increased expression of CD86 and reduced levels of CD206 and Arginase-1 (Figure 3D). PubMed:26675351
In hepatic and splenic macrophages, cotreatment with NAC or TAK-242 reduced the heme-induced upregulation of the M1 markers MHCII and CD86 and attenuated inducible nitric oxide synthase (iNOS) expression. PubMed:26675351
Cotreatment of M0 BMDMs with heme and TAK-242 attenuated the increase of the M1 markers MHCII, CD14, TNFα, IL-6, IL-1β, and CD86 and the decrease of the M2 marker CD206, IL-10, and Ym1 in comparison with heme treatment alone ( Figure 4A; supplemental Figures 5 and 12). PubMed:26675351
In addition, Hx and DFO prevented the heme- and ironmediated induction of the M1 markers MHCII, CD86, CD14, and TNFα and the decrease of some M2 markers, such as CD206, IL-10, and Arginase-1 (the last for FeNTA only) in M0 BMDMs (Figure 6A; supplemental Figure 15A). PubMed:26675351
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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.