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- W2013473815 abstract "Summary In our previous studies, the recombinant type II macrophage migration inhibitory factor homologue (r A s‐ MIF ) secreted from A nisakis simplex suppressed experimental inflammation mouse model through IL ‐10 production and CD 4 + CD 25 + F oxp3 + T ‐cell recruitment. Also, TLR 2 gene expression was significantly increased following r A s‐ MIF treatment. To know the relation between TLR 2 and amelioration mechanisms of r A s‐ MIF , we induced allergic airway inflammation by ovalbumin and alum with or without r A s‐ MIF under TLR 2 blocking systems [anti‐ TLR 2‐specific antibody (α‐m TLR 2 Ab) treatment and using TLR 2 knockout mice]. As a result, the amelioration effects of r A s‐ MIF in allergic airway inflammation model (diminished inflammation and T h2 response in the lung, increased IL ‐10 secretion, CD 4 + CD 25 + F oxp3 + T ‐cell recruitment) were diminished under two of the TLR 2 blocking model. The expression of TLR 2 on the surface of lung epithelial cell was significantly elevated by r A s‐ MIF treatment or P am3 CSK ( TLR 2‐specific agonist) treatment, but they might have some competition effect on the elevation of TLR 2 expression. In addition, the elevation of IL ‐10 gene expression by r A s‐ MIF treatment was significantly inhibited by α‐m TLR 2 Ab or P am3 CSK pretreatment. In conclusion, anti‐inflammatory effects of the r A s‐ MIF on OVA ‐induced allergic airway inflammation might be closely related to TLR 2." @default.
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- W2013473815 date "2015-03-11" @default.
- W2013473815 modified "2023-10-03" @default.
- W2013473815 title "TLR2-dependent amelioration of allergic airway inflammation by parasitic nematode type II MIF in mice" @default.
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- W2013473815 doi "https://doi.org/10.1111/pim.12172" @default.
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