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논문분류	춘계학술대회 초록집
제목	How to promote regeneration after ischemic reperfusion Injury: Dual role of CD 137 agonistic antibody
저자	*Jong soo LEE1, Jongha PARK1, Hojong PARK2, Kyung sun PARK1, Hong rae CHO2, Hyun chul CHUNG1
출판정보	2017; 2017(1):
키워드	ischemia reperfusion injury, AKI, regeneration
초록	Objectives : Acute sterile inflammation can be induced by tissue damage caused by ischemia-reperfusion. In transplantation ischemia reperfusion injury (IRI) is unavoidable procedure. IRI causes delayed graft function and increases rejection rates, finally shortens long-term graft survival. Previously we reported an inflammatory loop between tubular epithelial cells (TECs) and inflammatory cells during kidney IRI. Blocking this pathway demonstrated attenuating the severity of AKI. Although sterile inflammation plays a dominant role in damaging TECs in the early injury phase of AKI, blocking this inflammatory pathway may turn out the signal of the regeneration. Methods : We adopted mouse kidney ischemic reperfusion injury model. CD137-/- and CD137L-/- C57BL/6 mice were used between 7 and 8 weeks of age. Results : Here, we focused on CD 137 – CD137 ligand and reverse pathway which plays a dual role in both early inflammatory and late regenerative phase. In the early phase of IRI, CD 137 ligand signal on tubular epithelial cell amplifies inflammation and augments the intensity of tubular damage. During the healing phase, CD 137 signal promote regeneration of TEC by decreasing G2-M arrest of TEC, switching proinflammatory M1 macrophage to M2 macrophage, and expansion of regulatory T cell. Early administration of CD 137 agonistic antibody decreases the intensity of TEC injury via blocking CD 137 ligand signal of TEC. In addition, delayed treatment with CD 137 agonistic antibody promotes regeneration via enhancing CD 137 regenerative signal of immune cell Conclusions : In this work we provide evidence that treatment with CD 137 agonistic antibody can protect from IRI and its’ progression to chronic graft dysfunction by attenuating AKI severity and promoting regeneration of damaged tissue.
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