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Conference Paper: Δ42PD-1 expressed M2 macrophages promoted tumor recurrence after liver transplantation

TitleΔ42PD-1 expressed M2 macrophages promoted tumor recurrence after liver transplantation
Authors
Issue Date2018
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.transplantjournal.com
Citation
The 2018 Joint International Congress of ILTS, ELITA & LICAGE, Lisbon, Portugal, 23-26 May 2018. In Transplantation, 2018, v. 102 n. 5S, p. 7-8, abstract no. O-005 How to Cite?
AbstractΔ42PD-1 expressed M2 macrophages promoted tumor recurrence after liver transplantation Introduction Tumor recurrence remains to be a major challenge for liver transplantation for the patients with hepatocellular carcinoma. We previously reported that a subpopulation of macrophages (M2) led to poor recurrence-free survival in HCC patients received curative hepatectomy. The significances and activation mechanisms of these cells in liver transplantation are unknown. Preliminary evidences indicated the accumulation of a subset of M2 macrophages, expressed with Δ42PD-1, a natural isoform of a key immune regulator PD-1, in post-transplant tissues. We hypothesized that liver graft injury during transplantation may activate M2 macrophages, via Δ42PD-1 mechanism, lead to tumor recurrence. Materials and Methods In clinical study, the expressions level of intra-graft M2 macrophages with/without Δ42PD-1 were examined followed by the association analyses with patients’ post-transplant parameters. The tumor promoting mechanisms of M2 macrophages and Δ42PD-1 were investigated in rat tumor transplant model and in vitro co-cultivation studies. Results Clinically, 2.1-fold increased of intra-graft M2 macrophages were found in living donor compared to deceased donor liver transplantation (Figure-1). Moreover, Δ42PD-1 was found to be highly expressed in these cells (Figure-2). In terms of clinical significances, M2 macrophages contributed to the higher recurrence incidence and shorter recurrence-free survival in HCC recipients (Figure-3A-B). In vivo study showed that liver graft injuries significantly induced the accumulation of M2 macrophages after transplantation and resulted in larger tumor volume in the rat transplant tumor model (Figure-4). Δ42PD-1[high] macrophages expressed characteristic M2 phenotypes including pro-tumor cytokine secretory profiles compared to Δ42PD-1[low] cells. Conclusion We revealed a novel cellular mechanism of the post-transplant recurrence in liver transplantation. Liver graft injury induced the accumulation and activation of tumor promoting Δ42PD-1 M2 macrophages. Targeting the specific population represent a potential therapeutic strategy in attenuating HCC tumor recurrence.
Persistent Identifierhttp://hdl.handle.net/10722/263592
ISSN
2019 Impact Factor: 4.264
2015 SCImago Journal Rankings: 1.699

 

DC FieldValueLanguage
dc.contributor.authorYeung, WHO-
dc.contributor.authorLiu, L-
dc.contributor.authorChen, Z-
dc.contributor.authorLo, CM-
dc.contributor.authorMan, K-
dc.date.accessioned2018-10-22T07:41:25Z-
dc.date.available2018-10-22T07:41:25Z-
dc.date.issued2018-
dc.identifier.citationThe 2018 Joint International Congress of ILTS, ELITA & LICAGE, Lisbon, Portugal, 23-26 May 2018. In Transplantation, 2018, v. 102 n. 5S, p. 7-8, abstract no. O-005-
dc.identifier.issn0041-1337-
dc.identifier.urihttp://hdl.handle.net/10722/263592-
dc.description.abstractΔ42PD-1 expressed M2 macrophages promoted tumor recurrence after liver transplantation Introduction Tumor recurrence remains to be a major challenge for liver transplantation for the patients with hepatocellular carcinoma. We previously reported that a subpopulation of macrophages (M2) led to poor recurrence-free survival in HCC patients received curative hepatectomy. The significances and activation mechanisms of these cells in liver transplantation are unknown. Preliminary evidences indicated the accumulation of a subset of M2 macrophages, expressed with Δ42PD-1, a natural isoform of a key immune regulator PD-1, in post-transplant tissues. We hypothesized that liver graft injury during transplantation may activate M2 macrophages, via Δ42PD-1 mechanism, lead to tumor recurrence. Materials and Methods In clinical study, the expressions level of intra-graft M2 macrophages with/without Δ42PD-1 were examined followed by the association analyses with patients’ post-transplant parameters. The tumor promoting mechanisms of M2 macrophages and Δ42PD-1 were investigated in rat tumor transplant model and in vitro co-cultivation studies. Results Clinically, 2.1-fold increased of intra-graft M2 macrophages were found in living donor compared to deceased donor liver transplantation (Figure-1). Moreover, Δ42PD-1 was found to be highly expressed in these cells (Figure-2). In terms of clinical significances, M2 macrophages contributed to the higher recurrence incidence and shorter recurrence-free survival in HCC recipients (Figure-3A-B). In vivo study showed that liver graft injuries significantly induced the accumulation of M2 macrophages after transplantation and resulted in larger tumor volume in the rat transplant tumor model (Figure-4). Δ42PD-1[high] macrophages expressed characteristic M2 phenotypes including pro-tumor cytokine secretory profiles compared to Δ42PD-1[low] cells. Conclusion We revealed a novel cellular mechanism of the post-transplant recurrence in liver transplantation. Liver graft injury induced the accumulation and activation of tumor promoting Δ42PD-1 M2 macrophages. Targeting the specific population represent a potential therapeutic strategy in attenuating HCC tumor recurrence.-
dc.languageeng-
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.transplantjournal.com-
dc.relation.ispartofTransplantation-
dc.relation.ispartofThe 2018 Joint International Congress of ILTS, ELITA & LICAGE-
dc.titleΔ42PD-1 expressed M2 macrophages promoted tumor recurrence after liver transplantation-
dc.typeConference_Paper-
dc.identifier.emailYeung, WHO: why21@hku.hk-
dc.identifier.emailLiu, L: liuli71@hkucc.hku.hk-
dc.identifier.emailChen, Z: zchenai@hku.hk-
dc.identifier.emailLo, CM: chungmlo@hkucc.hku.hk-
dc.identifier.emailMan, K: kwanman@hku.hk-
dc.identifier.authorityLiu, L=rp00268-
dc.identifier.authorityChen, Z=rp00243-
dc.identifier.authorityLo, CM=rp00412-
dc.identifier.authorityMan, K=rp00417-
dc.identifier.hkuros294569-
dc.identifier.volume102-
dc.identifier.issue5S-
dc.identifier.spage7-
dc.identifier.epage8-
dc.publisher.placeUnited States-

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