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Conference Paper: Δ42PD-1 expressed M2 macrophages promoted tumor recurrence after liver transplantation
Title | Δ42PD-1 expressed M2 macrophages promoted tumor recurrence after liver transplantation |
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Authors | |
Issue Date | 2018 |
Publisher | Lippincott 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? |
Abstract | Δ42PD-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 Identifier | http://hdl.handle.net/10722/263592 |
ISSN | 2023 Impact Factor: 5.3 2023 SCImago Journal Rankings: 1.371 |
DC Field | Value | Language |
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dc.contributor.author | Yeung, WHO | - |
dc.contributor.author | Liu, L | - |
dc.contributor.author | Chen, Z | - |
dc.contributor.author | Lo, CM | - |
dc.contributor.author | Man, K | - |
dc.date.accessioned | 2018-10-22T07:41:25Z | - |
dc.date.available | 2018-10-22T07:41:25Z | - |
dc.date.issued | 2018 | - |
dc.identifier.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 | - |
dc.identifier.issn | 0041-1337 | - |
dc.identifier.uri | http://hdl.handle.net/10722/263592 | - |
dc.description.abstract | Δ42PD-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.language | eng | - |
dc.publisher | Lippincott Williams & Wilkins. The Journal's web site is located at http://www.transplantjournal.com | - |
dc.relation.ispartof | Transplantation | - |
dc.relation.ispartof | The 2018 Joint International Congress of ILTS, ELITA & LICAGE | - |
dc.title | Δ42PD-1 expressed M2 macrophages promoted tumor recurrence after liver transplantation | - |
dc.type | Conference_Paper | - |
dc.identifier.email | Yeung, WHO: why21@hku.hk | - |
dc.identifier.email | Liu, L: liuli71@hkucc.hku.hk | - |
dc.identifier.email | Chen, Z: zchenai@hku.hk | - |
dc.identifier.email | Lo, CM: chungmlo@hkucc.hku.hk | - |
dc.identifier.email | Man, K: kwanman@hku.hk | - |
dc.identifier.authority | Liu, L=rp00268 | - |
dc.identifier.authority | Chen, Z=rp00243 | - |
dc.identifier.authority | Lo, CM=rp00412 | - |
dc.identifier.authority | Man, K=rp00417 | - |
dc.identifier.hkuros | 294569 | - |
dc.identifier.volume | 102 | - |
dc.identifier.issue | 5S | - |
dc.identifier.spage | 7 | - |
dc.identifier.epage | 8 | - |
dc.publisher.place | United States | - |
dc.identifier.issnl | 0041-1337 | - |