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NOD2 , as an innate sensor, participates in IL-1 maturation and amplification of the inflammatory response (104), while AGER promotes asthmatic inflammation by stimulating IL33 -dependent activation of type-2 innate lymphoid cells (105)

However, this observation may be attributed to the regulation of Tim-3-expressing dendritic cells and/or regulatory T cells, suggesting that CD8 T cell function was indirectly enhanced upon anti-Tim-3 therapy in mice [38,39,40]

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In contrast, the expression of IGFBP-1 and IGFBP-5 mRNAs starts to increase 72 h after muscle damage and is similar to those of p21 and myogenin mRNAs which are mainly involved in myogenic differentiation[83]