Early Posttransplant Mobilization of Monocytic Myeloid-derived Suppressor Cell Correlates With Increase in Soluble Immunosuppressive Factors and Predicts Cancer in Kidney Recipients.


Journal

Transplantation
ISSN: 1534-6080
Titre abrégé: Transplantation
Pays: United States
ID NLM: 0132144

Informations de publication

Date de publication:
12 2020
Historique:
pubmed: 19 2 2020
medline: 9 2 2021
entrez: 19 2 2020
Statut: ppublish

Résumé

Myeloid-derived suppressor cells (MDSCs) increase in patients with cancer and are associated with poor prognosis; however, their role in transplantation is not yet understood. Here we aimed to study the MDSC effects on the evolution of kidney transplant recipients (KTRs). A cohort of 229 KTRs was prospectively analyzed. Two myeloid cells subsets. CD11bCD33CD14CD15HLA-DR (monocytic MDSC [M-MDSC]) and CD11bCD33CD14CD15HLA-DR (monocytes), were defined by flow cytometry. The suppressive capacity of myeloid cells was tested in cocultures with autologous lymphocytes. Suppressive soluble factors, cytokines, anti-HLA antibodies, and total antioxidant capacity were quantified in plasma. Pretransplant, M-MDSC, and monocytes were similar in KTRs and healthy volunteers. M-MDSCs increased immediately posttransplantation and suppressed CD4 and CD8 T cells proliferation. M-MDSCs remained high for 1 y posttransplantation. Higher M-MDSC counts at day 14 posttransplant were observed in patients who subsequently developed cancer, and KTRs with higher M-MDSC at day 14 had significantly lower malignancy-free survival. Day 14 M-MDSC >179.2 per microliter conferred 6.98 times (95% confidence interval, 1.28-37.69) more risk to develop cancer, independently from age, gender, and immunosuppression. Early posttransplant M-MDSCs were lower in patients with enhanced alloimmune response as represented by anti-HLA sensitization. M-MDSC counts correlated with higher circulatory suppressive factors arginase-1 and interleukin-10, and lower total antioxidant capacity. Early posttransplant mobilization of M-MDSCs predicts cancer and adds risk as an independent factor. M-MDSC may favor an immunosuppressive environment that promotes tumoral development.

Sections du résumé

BACKGROUND
Myeloid-derived suppressor cells (MDSCs) increase in patients with cancer and are associated with poor prognosis; however, their role in transplantation is not yet understood. Here we aimed to study the MDSC effects on the evolution of kidney transplant recipients (KTRs).
METHODS
A cohort of 229 KTRs was prospectively analyzed. Two myeloid cells subsets. CD11bCD33CD14CD15HLA-DR (monocytic MDSC [M-MDSC]) and CD11bCD33CD14CD15HLA-DR (monocytes), were defined by flow cytometry. The suppressive capacity of myeloid cells was tested in cocultures with autologous lymphocytes. Suppressive soluble factors, cytokines, anti-HLA antibodies, and total antioxidant capacity were quantified in plasma.
RESULTS
Pretransplant, M-MDSC, and monocytes were similar in KTRs and healthy volunteers. M-MDSCs increased immediately posttransplantation and suppressed CD4 and CD8 T cells proliferation. M-MDSCs remained high for 1 y posttransplantation. Higher M-MDSC counts at day 14 posttransplant were observed in patients who subsequently developed cancer, and KTRs with higher M-MDSC at day 14 had significantly lower malignancy-free survival. Day 14 M-MDSC >179.2 per microliter conferred 6.98 times (95% confidence interval, 1.28-37.69) more risk to develop cancer, independently from age, gender, and immunosuppression. Early posttransplant M-MDSCs were lower in patients with enhanced alloimmune response as represented by anti-HLA sensitization. M-MDSC counts correlated with higher circulatory suppressive factors arginase-1 and interleukin-10, and lower total antioxidant capacity.
CONCLUSIONS
Early posttransplant mobilization of M-MDSCs predicts cancer and adds risk as an independent factor. M-MDSC may favor an immunosuppressive environment that promotes tumoral development.

Identifiants

pubmed: 32068661
doi: 10.1097/TP.0000000000003179
pii: 00007890-202012000-00026
doi:

Substances chimiques

Immunosuppressive Agents 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2599-2608

Références

Liu W, Xiao X, Demirci G, et al. Innate NK cells and macrophages recognize and reject allogeneic nonself in vivo via different mechanisms. J Immunol. 2012; 188:2703–2711. doi: 10.4049/jimmunol.1102997
doi: 10.4049/jimmunol.1102997
Ochando J, Kwan WH, Ginhoux F, et al. The mononuclear phagocyte system in organ transplantation. Am J Transplant. 2016; 16:1053–1069. doi: 10.1111/ajt.13627
doi: 10.1111/ajt.13627
Hancock WW, Thomson NM, Atkins RC. Composition of interstitial cellular infiltrate identified by monoclonal antibodies in renal biopsies of rejecting human renal allografts. Transplantation. 1983; 35:458–463. doi: 10.1097/00007890-198305000-00013
doi: 10.1097/00007890-198305000-00013
Thomas J, Thomas F, Hoffmann S, et al. Macrophage-related suppressor cells in human renal transplant recipients. Surgery. 1979; 86:266–274
Conde P, Rodriguez M, van der Touw W, et al. DC-SIGN(+) macrophages control the induction of transplantation tolerance. Immunity. 2015; 42:1143–1158. doi: 10.1016/j.immuni.2015.05.009
doi: 10.1016/j.immuni.2015.05.009
Dugast AS, Haudebourg T, Coulon F, et al. Myeloid-derived suppressor cells accumulate in kidney allograft tolerance and specifically suppress effector T cell expansion. J Immunol. 2008; 180:7898–7906. doi: 10.4049/jimmunol.180.12.7898
doi: 10.4049/jimmunol.180.12.7898
Garcia MR, Ledgerwood L, Yang Y, et al. Monocytic suppressive cells mediate cardiovascular transplantation tolerance in mice. J Clin Invest. 2010; 120:2486–2496. doi: 10.1172/JCI41628
doi: 10.1172/JCI41628
Gray CM, Smit JA, Myburgh JA. Identification of non-T suppressor cells with possible contra-interleukin-2 properties in non-human primates tolerant to their renal allograft. Afr J Health Sci. 1995; 2:354–358
Gabrilovich DI, Nagaraj S. Myeloid-derived suppressor cells as regulators of the immune system. Nat Rev Immunol. 2009; 9:162–174. doi: 10.1038/nri2506
doi: 10.1038/nri2506
Bronte V, Brandau S, Chen SH, et al. Recommendations for myeloid-derived suppressor cell nomenclature and characterization standards. Nat Commun. 2016; 7:12150. doi: 10.1038/ncomms12150
doi: 10.1038/ncomms12150
Musolino C, Allegra A, Pioggia G, et al. Immature myeloid-derived suppressor cells: a bridge between inflammation and cancer (review). Oncol Rep. 2017; 37:671–683. doi: 10.3892/or.2016.5291
doi: 10.3892/or.2016.5291
Ochando J, Conde P, Utrero-Rico A, et al. Tolerogenic role of myeloid suppressor cells in organ transplantation. Front Immunol. 2019; 10:374. doi: 10.3389/fimmu.2019.00374
doi: 10.3389/fimmu.2019.00374
Riquelme P, Haarer J, Kammler A, et al. TIGIT+ iTregs elicited by human regulatory macrophages control T cell immunity. Nat Commun. 2018; 9:2858. doi: 10.1038/s41467-018-05167-8
doi: 10.1038/s41467-018-05167-8
Du XX, Guo YL, Zhao YP, et al. Accumulation of high levels of monocytic myeloid-derived suppressor cells enhances graft survival in almost-tolerant kidney transplant recipients. Transplant Proc. 2018; 50:3314–3320. doi: 10.1016/j.transproceed.2018.04.043
doi: 10.1016/j.transproceed.2018.04.043
Hock BD, Mackenzie KA, Cross NB, et al. Renal transplant recipients have elevated frequencies of circulating myeloid-derived suppressor cells. Nephrol Dial Transplant. 2012; 27:402–410. doi: 10.1093/ndt/gfr264
doi: 10.1093/ndt/gfr264
Hock BD, McKenzie JL, Cross NB, et al. Dynamic changes in myeloid derived suppressor cell subsets following renal transplant: a prospective study. Transpl Immunol. 2015; 32:164–171. doi: 10.1016/j.trim.2015.05.001
doi: 10.1016/j.trim.2015.05.001
Luan Y, Mosheir E, Menon MC, et al. Monocytic myeloid-derived suppressor cells accumulate in renal transplant patients and mediate CD4(+) Foxp3(+) Treg expansion. Am J Transplant. 2013; 13:3123–3131. doi: 10.1111/ajt.12461
doi: 10.1111/ajt.12461
Meng F, Chen S, Guo X, et al. Clinical significance of myeloid-derived suppressor cells in human renal transplantation with acute T cell-mediated rejection. Inflammation. 2014; 37:1799–1805. doi: 10.1007/s10753-014-9910-5
doi: 10.1007/s10753-014-9910-5
Saleh L, Plieth C. Total low-molecular-weight antioxidants as a summary parameter, quantified in biological samples by a chemiluminescence inhibition assay. Nat Protoc. 2010; 5:1627–1634. doi: 10.1038/nprot.2010.120
doi: 10.1038/nprot.2010.120
Okano S, Abu-Elmagd K, Kish DD, et al. Myeloid-derived suppressor cells increase and inhibit donor-reactive T cell responses to graft intestinal epithelium in intestinal transplant patients. Am J Transplant. 2018; 18:2544–2558. doi: 10.1111/ajt.14718
doi: 10.1111/ajt.14718
Au E, Wong G, Chapman JR. Cancer in kidney transplant recipients. Nat Rev Nephrol. 2018; 14:508–520. doi: 10.1038/s41581-018-0022-6
doi: 10.1038/s41581-018-0022-6
Haas M, Sis B, Racusen LC, et al.; Banff meeting report writing committee. Banff 2013 meeting report: inclusion of c4d-negative antibody-mediated rejection and antibody-associated arterial lesions. Am J Transplant. 2014; 14:272–283. doi: 10.1111/ajt.12590
doi: 10.1111/ajt.12590
Schmid MC, Khan SQ, Kaneda MM, et al. Integrin CD11B activation drives anti-tumor innate immunity. Nat Commun. 2018; 9:5379. doi: 10.1038/s41467-018-07387-4
doi: 10.1038/s41467-018-07387-4
Birben E, Sahiner UM, Sackesen C, et al. Oxidative stress and antioxidant defense. World Allergy Organ J. 2012; 5:9–19. doi: 10.1097/WOX.0b013e3182439613
doi: 10.1097/WOX.0b013e3182439613
Griendling KK, Touyz RM, Zweier JL, et al.; American Heart Association Council on Basic Cardiovascular Sciences. Measurement of reactive oxygen species, reactive nitrogen species, and redox-dependent signaling in the cardiovascular system: a scientific statement from the American Heart Association. Circ Res. 2016; 119:e39–e75. doi: 10.1161/RES.0000000000000110
doi: 10.1161/RES.0000000000000110
Zhang R, Shi J, Zhang R, et al. Expanded CD14HICD16- immunosuppressive monocytes predict disease severity in patients with acute pancreatitis. J Immunol. 2019; 202:2578–2584. doi: 10.4049/jimmunol.1801194
doi: 10.4049/jimmunol.1801194
Suk Lee Y, Davila E, Zhang T, et al. Myeloid-derived suppressor cells are bound and inhibited by anti-thymocyte globulin. Innate Immun. 2019; 25:46–59. doi: 10.1177/1753425918820427
doi: 10.1177/1753425918820427
Chiasson VL, Bounds KR, Chatterjee P, et al. Myeloid-derived suppressor cells ameliorate cyclosporine A-induced hypertension in mice. Hypertension. 2018; 71:199–207. doi: 10.1161/HYPERTENSIONAHA.117.10306
doi: 10.1161/HYPERTENSIONAHA.117.10306
Han C, Wu T, Na N, et al. The effect of immunosuppressive drug cyclosporine A on myeloid-derived suppressor cells in transplanted mice. Inflamm Res. 2016; 65:679–688. doi: 10.1007/s00011-016-0949-7
doi: 10.1007/s00011-016-0949-7
Wang Y, Ding Y, Guo N, et al. MDSCs: key criminals of tumor pre-metastatic niche formation. Front Immunol. 2019; 10:172. doi: 10.3389/fimmu.2019.00172
doi: 10.3389/fimmu.2019.00172
Yan HH, Pickup M, Pang Y, et al. Gr-1+CD11B+ myeloid cells tip the balance of immune protection to tumor promotion in the premetastatic lung. Cancer Res. 2010; 70:6139–6149. doi: 10.1158/0008-5472.CAN-10-0706
doi: 10.1158/0008-5472.CAN-10-0706
Dantal J, Hourmant M, Cantarovich D, et al. Effect of long-term immunosuppression in kidney-graft recipients on cancer incidence: randomised comparison of two cyclosporin regimens. Lancet. 1998; 351:623–628. doi: 10.1016/S0140-6736(97)08496-1
doi: 10.1016/S0140-6736(97)08496-1
Grulich AE, van Leeuwen MT, Falster MO, et al. Incidence of cancers in people with HIV/AIDS compared with immunosuppressed transplant recipients: a meta-analysis. Lancet. 2007; 370:59–67. doi: 10.1016/S0140-6736(07)61050-2
doi: 10.1016/S0140-6736(07)61050-2
van Leeuwen MT, Webster AC, McCredie MR, et al. Effect of reduced immunosuppression after kidney transplant failure on risk of cancer: population based retrospective cohort study. BMJ. 2010; 340:c570. doi: 10.1136/bmj.c570
doi: 10.1136/bmj.c570
Hall EC, Engels EA, Pfeiffer RM, et al. Association of antibody induction immunosuppression with cancer after kidney transplantation. Transplantation. 2015; 99:1051–1057. doi: 10.1097/TP.0000000000000449
doi: 10.1097/TP.0000000000000449
Lim WH, Turner RM, Chapman JR, et al. Acute rejection, T-cell-depleting antibodies, and cancer after transplantation. Transplantation. 2014; 97:817–825. doi: 10.1097/01.TP.0000442773.38510.32
doi: 10.1097/01.TP.0000442773.38510.32
Opelz G, Naujokat C, Daniel V, et al. Disassociation between risk of graft loss and risk of non-hodgkin lymphoma with induction agents in renal transplant recipients. Transplantation. 2006; 81:1227–1233. doi: 10.1097/01.tp.0000219817.18049.36
doi: 10.1097/01.tp.0000219817.18049.36
Fernández-Ruiz M, López-Medrano F, Allende LM, et al. Assessing the risk of de novo malignancy in kidney transplant recipients: role for monitoring of peripheral blood lymphocyte populations. Transplantation. 2014; 98:e36–e37. doi: 10.1097/TP.0000000000000297
doi: 10.1097/TP.0000000000000297
Hope CM, Troelnikov A, Hanf W, et al. Peripheral natural killer cell and allo-stimulated T-cell function in kidney transplant recipients associate with cancer risk and immunosuppression-related complications. Kidney Int. 2015; 88:1374–1382. doi: 10.1038/ki.2015.237
doi: 10.1038/ki.2015.237
Bottomley MJ, Harden PN, Wood KJ. CD8+ immunosenescence predicts post-transplant cutaneous squamous cell carcinoma in high-risk patients. J Am Soc Nephrol. 2016; 27:1505–1515. doi: 10.1681/ASN.2015030250
doi: 10.1681/ASN.2015030250
Carroll RP, Segundo DS, Hollowood K, et al. Immune phenotype predicts risk for posttransplantation squamous cell carcinoma. J Am Soc Nephrol. 2010; 21:713–722. doi: 10.1681/ASN.2009060669
doi: 10.1681/ASN.2009060669
Hope CM, Grace BS, Pilkington KR, et al. The immune phenotype may relate to cancer development in kidney transplant recipients. Kidney Int. 2014; 86:175–183. doi: 10.1038/ki.2013.538
doi: 10.1038/ki.2013.538
Beury DW, Parker KH, Nyandjo M, et al. Cross-talk among myeloid-derived suppressor cells, macrophages, and tumor cells impacts the inflammatory milieu of solid tumors. J Leukoc Biol. 2014; 96:1109–1118. doi: 10.1189/jlb.3A0414-210R
doi: 10.1189/jlb.3A0414-210R
Highfill SL, Rodriguez PC, Zhou Q, et al. Bone marrow myeloid-derived suppressor cells (MDSCs) inhibit graft-versus-host disease (GVHD) via an arginase-1-dependent mechanism that is up-regulated by interleukin-13. Blood. 2010; 116:5738–5747. doi: 10.1182/blood-2010-06-287839
doi: 10.1182/blood-2010-06-287839
Sinha P, Clements VK, Bunt SK, et al. Cross-talk between myeloid-derived suppressor cells and macrophages subverts tumor immunity toward a type 2 response. J Immunol. 2007; 179:977–983. doi: 10.4049/jimmunol.179.2.977
doi: 10.4049/jimmunol.179.2.977
Youn JI, Gabrilovich DI. The biology of myeloid-derived suppressor cells: the blessing and the curse of morphological and functional heterogeneity. Eur J Immunol. 2010; 40:2969–2975. doi: 10.1002/eji.201040895
doi: 10.1002/eji.201040895
Lee SE, Lim JY, Kim TW, et al. Matrix metalloproteinase-9 in monocytic myeloid-derived suppressor cells correlate with early infections and clinical outcomes in allogeneic hematopoietic stem cell transplantation. Biol Blood Marrow Transplant. 2018; 24:32–42. doi: 10.1016/j.bbmt.2017.08.017
doi: 10.1016/j.bbmt.2017.08.017
Mackert JR, Qu P, Min Y, et al. Dual negative roles of C/EBPα in the expansion and pro-tumor functions of MDSCs. Sci Rep. 2017; 7:14048. doi: 10.1038/s41598-017-12968-2
doi: 10.1038/s41598-017-12968-2
Zhang W, Liang S, Wu J, et al. Human inhibitory receptor immunoglobulin-like transcript 2 amplifies CD11B+Gr1+ myeloid-derived suppressor cells that promote long-term survival of allografts. Transplantation. 2008; 86:1125–1134. doi: 10.1097/TP.0b013e318186fccd
doi: 10.1097/TP.0b013e318186fccd
De Wilde V, Van Rompaey N, Hill M, et al. Endotoxin-induced myeloid-derived suppressor cells inhibit alloimmune responses via heme oxygenase-1. Am J Transplant. 2009; 9:2034–2047. doi: 10.1111/j.1600-6143.2009.02757.x
doi: 10.1111/j.1600-6143.2009.02757.x
Rekers NV, Bajema IM, Mallat MJ, et al. Beneficial immune effects of myeloid-related proteins in kidney transplant rejection. Am J Transplant. 2016; 16:1441–1455. doi: 10.1111/ajt.13634
doi: 10.1111/ajt.13634
Di Giacomo C, Acquaviva R, Lanteri R, et al. Nonproteic antioxidant status in plasma of subjects with colon cancer. Exp Biol Med (Maywood). 2003; 228:525–528. doi: 10.1177/15353702-0322805-17
doi: 10.1177/15353702-0322805-17
Korde SD, Basak A, Chaudhary M, et al. Enhanced nitrosative and oxidative stress with decreased total antioxidant capacity in patients with oral precancer and oral squamous cell carcinoma. Oncology. 2011; 80:382–389. doi: 10.1159/000329811
doi: 10.1159/000329811

Auteurs

Alberto Utrero-Rico (A)

Immunodeficiencies and Transplant Immunology Group, Instituto de Investigación Sanitaria Hospital Universitario 12 de Octubre (imas 12), Madrid, Spain.

Rocio Laguna-Goya (R)

Immunodeficiencies and Transplant Immunology Group, Instituto de Investigación Sanitaria Hospital Universitario 12 de Octubre (imas 12), Madrid, Spain.
Department of Immunology, Hospital Universitario 12 de Octubre, Madrid, Spain.

Francisco Cano-Romero (F)

Immunodeficiencies and Transplant Immunology Group, Instituto de Investigación Sanitaria Hospital Universitario 12 de Octubre (imas 12), Madrid, Spain.

Marta Chivite-Lacaba (M)

Immunodeficiencies and Transplant Immunology Group, Instituto de Investigación Sanitaria Hospital Universitario 12 de Octubre (imas 12), Madrid, Spain.

Cecilia Gonzalez-Cuadrado (C)

Immunodeficiencies and Transplant Immunology Group, Instituto de Investigación Sanitaria Hospital Universitario 12 de Octubre (imas 12), Madrid, Spain.

Elena Rodríguez-Sánchez (E)

Cardiorenal Translational Laboratory, imas12, Madrid, Spain.

Gema Ruiz-Hurtado (G)

Cardiorenal Translational Laboratory, imas12, Madrid, Spain.
CIBER-CV, Hospital Universitario 12 de Octubre, Madrid, Spain.

Antonio Serrano (A)

Immunodeficiencies and Transplant Immunology Group, Instituto de Investigación Sanitaria Hospital Universitario 12 de Octubre (imas 12), Madrid, Spain.
Department of Immunology, Hospital Universitario 12 de Octubre, Madrid, Spain.

Mario Fernández-Ruiz (M)

Immunodeficiencies and Transplant Immunology Group, Instituto de Investigación Sanitaria Hospital Universitario 12 de Octubre (imas 12), Madrid, Spain.
Unit of Infectious Diseases, Hospital Universitario 12 de Octubre, Madrid, Spain.

Iago Justo (I)

Department of Surgery and Abdominal Organs Transplantation, Hospital Universitario 12 de Octubre, Madrid, Spain.

Esther González (E)

Department of Nephrology, Hospital Universitario 12 de Octubre, Madrid, Spain.

Amado Andrés (A)

Department of Nephrology, Hospital Universitario 12 de Octubre, Madrid, Spain.

Estela Paz-Artal (E)

Immunodeficiencies and Transplant Immunology Group, Instituto de Investigación Sanitaria Hospital Universitario 12 de Octubre (imas 12), Madrid, Spain.
Department of Immunology, Hospital Universitario 12 de Octubre, Madrid, Spain.
Department of Immunology, Oftalmology and ENT, Universidad Complutense de Madrid, Madrid, Spain.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH