scholarly journals How I treat EBV lymphoproliferation

Blood ◽  
2009 ◽  
Vol 114 (19) ◽  
pp. 4002-4008 ◽  
Author(s):  
Helen E. Heslop
Keyword(s):  
B Cells ◽  
Cytotoxic T Lymphocyte ◽  
Cytotoxic T Cells ◽  
Treatment Options ◽  
Solid Organ Transplantation ◽  
Solid Organ ◽  
Hematopoietic Stem ◽  
Serial Measurement ◽  
Barr Virus ◽  
Epstein Barr

Abstract Epstein-Barr virus (EBV)–associated B-cell lymphoproliferation is a life-threatening complication after hematopoietic stem cell or solid organ transplantation resulting from outgrowth of EBV-infected B cells that would normally be controlled by EBV-cytotoxic T cells. During the past decade, early detection strategies, such as serial measurement of EBV-DNA load in peripheral blood samples, have helped to identify high-risk patients and to diagnose early lymphoproliferation. Treatment options include manipulation of the balance between outgrowing EBV-infected B cells and the EBV cytotoxic T lymphocyte response and targeting the B cells with monoclonal antibodies or chemotherapy. Major challenges remain for defining indications for preemptive therapies and integrating novel and conventional therapies.

scholarly journals Analysis of Post-Transplant Lymphoproliferative Disorder (PTLD) Outcomes with Epstein–Barr Virus (EBV) Assessments—A Single Tertiary Referral Center Experience and Review of Literature

Cancers ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 899
Author(s):  
Eric Lau ◽  
Justin Tyler Moyers ◽  
Billy Chen Wang ◽  
Il Seok Daniel Jeong ◽  
Joanne Lee ◽  
...  
Keyword(s):  
Epstein Barr Virus ◽  
Solid Organ Transplantation ◽  
Solid Organ ◽  
Allogeneic Bone ◽  
Hematopoietic Stem ◽  
Tertiary Referral Center ◽  
Post Transplant ◽  
Barr Virus ◽  
Significant Difference ◽  
Epstein Barr

Post-transplant lymphoproliferative disorders (PTLDs) are lymphoid or plasmacytic proliferations ranging from polyclonal reactive proliferations to overt lymphomas that develop as consequence of immunosuppression in recipients of solid organ transplantation (SOT) or allogeneic bone marrow/hematopoietic stem cell transplantation. Immunosuppression and Epstein–Barr virus (EBV) infection are known risk factors for PTLD. Patients with documented histopathologic diagnosis of primary PTLD at our institution between January 2000 and October 2019 were studied. Sixty-six patients with PTLD following SOT were followed for a median of 9.0 years. The overall median time from transplant to PTLD diagnosis was 5.5 years, with infant transplants showing the longest time to diagnosis at 12.0 years, compared to pediatric and adolescent transplants at 4.0 years and adult transplants at 4.5 years. The median overall survival (OS) was 19.0 years. In the monomorphic diffuse large B-cell (M-DLBCL-PTLD) subtype, median OS was 10.7 years, while median OS for polymorphic subtype was not yet reached. There was no significant difference in OS in patients with M-DLBCL-PTLD stratified by quantitative EBV viral load over and under 100,000 copies/mL at time of diagnosis, although there was a trend towards worse prognosis in those with higher copies.

Generation of EBV-specific cytotoxic T cells that are resistant to calcineurin inhibitors for the treatment of posttransplantation lymphoproliferative disease

Blood ◽  
2009 ◽  
Vol 114 (23) ◽  
pp. 4792-4803 ◽  
Author(s):  
Jennifer Brewin ◽  
Christoph Mancao ◽  
Karin Straathof ◽  
Helen Karlsson ◽  
Sujith Samarasinghe ◽  
...  
Keyword(s):  
Cytotoxic T Cells ◽  
Solid Organ Transplantation ◽  
Calcineurin Inhibitors ◽  
Interferon Γ ◽  
Lymphoproliferative Disease ◽  
Solid Organ ◽  
Vector Coding ◽  
Barr Virus ◽  
The Face ◽  
Epstein Barr

AbstractEpstein-Barr virus (EBV)–driven posttransplantation lymphoproliferative disease (PTLD) is a serious complication of immunosuppression after either stem cell transplantation (SCT) or solid organ transplantation (SOT). Adoptive transfer of EBV-specific cytotoxic T lymphocytes (EBV-CTLs) is an effective prophylaxis and treatment for PTLD after SCT, but not for PTLD after SOT when pharmacologic immunosuppression cannot be discontinued. We report the generation of calcineurin (CN) mutants that render EBV-CTL resistant to the immunosuppressants tacrolimus (FK506) and cyclosporin A (CsA): mutant CNa12 confers resistance to CsA but not FK506, and mutant CNa22 confers resistance to FK506 but not CsA, whereas mutant CNb30 renders CTLs resistant to both calcineurin inhibitors. Untransduced EBV-CTLs do not proliferate in the presence of FK506/CsA. However, EBV-CTLs transduced with a retroviral vector coding for these mutants retain the ability to both proliferate and secrete normal levels of interferon-γ in the presence therapeutic levels of FK506 (CNa12), CsA (CNa22), or both (CNb30). The cytotoxicity and phenotype of EBV-CTL lines were unaffected by expression of these mutant CNs. This approach should allow effective immunotherapy with EBV-CTLs in the SOT setting without risking the graft by reduction in immunosuppression, and represents a generic approach to improving immunotherapy in the face of immunosuppression.

scholarly journals Lymphoma of the lip after kidney transplantation: a case report

2019 ◽  
Vol 26 (1) ◽  
pp. 2
Author(s):  
Xavier Payet ◽  
Hélène Raybaud ◽  
Morgane Kipper ◽  
Enzo Fino ◽  
Christine Voha
Keyword(s):  
Immunosuppressive Treatment ◽  
Solid Organ Transplantation ◽  
Histopathological Analysis ◽  
Epstein Barr Virus Infection ◽  
Solid Organ ◽  
Hematopoietic Stem ◽  
Barr Virus ◽  
Non Hodgkin Lymphoma ◽  
Epstein Barr ◽  
Barr Virus Infection

Introduction: In transplant recipients, the risk to develop cancer increases 4 fold compared to general population due to the immunosuppressive treatment. Observation: A 68 years old woman, kidney transplanted four years ago, presented with a slowly growing swelling over her left lip since six weeks. The histopathological analyses showed a non Hodgkin lymphoma. Comment: Post-transplant lymphoproliferative disorders (PTLD) is a complication developing after solid organ transplantation or allogenic hematopoietic stem cell transplantation. Immunosuppression due to the immunosuppressives drugs is considered as the most important risk factor and the incidence rate depends of transplant type, age and risk of primary Epstein-Barr virus infection. Conclusion: PTLD is a rare but serious complication. It must be suspected in all cases of intra-oral mass for a transplanted patient and requires a histopathological analysis for early diagnosis and appropriate treatment.

scholarly journals Selective Induction of Th2-Attracting Chemokines CCL17 and CCL22 in Human B Cells by Latent Membrane Protein 1 of Epstein-Barr Virus

2004 ◽  
Vol 78 (4) ◽  
pp. 1665-1674 ◽  
Author(s):  
Takashi Nakayama ◽  
Kunio Hieshima ◽  
Daisuke Nagakubo ◽  
Emiko Sato ◽  
Masahiro Nakayama ◽  
...  
Keyword(s):  
T Cells ◽  
B Cells ◽  
Regulatory T Cells ◽  
Epstein Barr Virus ◽  
Cytotoxic T Cells ◽  
Th2 Cells ◽  
Th1 Cells ◽  
Barr Virus ◽  
Ebv Infection ◽  
Epstein Barr

ABSTRACT Chemokines are likely to play important roles in the pathophysiology of diseases associated with Epstein-Barr virus (EBV). Here, we have analyzed the repertoire of chemokines expressed by EBV-infected B cells. EBV infection of B cells induced expression of TARC/CCL17 and MDC/CCL22, which are known to attract Th2 cells and regulatory T cells via CCR4, and also upregulated constitutive expression of MIP-1α/CCL3, MIP-1β/CCL4, and RANTES/CCL5, which are known to attract Th1 cells and cytotoxic T cells via CCR5. Accordingly, EBV-immortalized B cells secreted these chemokines, especially CCL3, CCL4, and CCL22, in large quantities. EBV infection or stable expression of LMP1 also induced CCL17 and CCL22 in a B-cell line, BJAB. The inhibitors of the TRAF/NF-κB pathway (BAY11-7082) and the p38/ATF2 pathway (SB202190) selectively suppressed the expression of CCL17 and CCL22 in EBV-immortalized B cells and BJAB-LMP1. Consistently, transient-transfection assays using CCL22 promoter-reporter constructs demonstrated that two NF-κB sites and a single AP-1 site were involved in the activation of the CCL22 promoter by LMP1. Finally, serum CCL22 levels were significantly elevated in infectious mononucleosis. Collectively, LMP1 induces CCL17 and CCL22 in EBV-infected B cells via activation of NF-κB and probably ATF2. Production of CCL17 and CCL22, which attract Th2 and regulatory T cells, may help EBV-infected B cells evade immune surveillance by Th1 cells. However, the concomitant production of CCL3, CCL4, and CCL5 by EBV-infected B cells may eventually attract Th1 cells and cytotoxic T cells, leading to elimination of EBV-infected B cells at latency III and to selection of those with limited expression of latent genes.

scholarly journals Epstein-Barr Virus–Positive Posttransplant Lymphoproliferative Disease After Solid Organ Transplantation

2016 ◽  
Vol 2 (1) ◽  
pp. e48 ◽  
Author(s):  
Marieke L. Nijland ◽  
Marie José Kersten ◽  
Steven T. Pals ◽  
Frederike J. Bemelman ◽  
Ineke J.M. ten Berge
Keyword(s):  
Organ Transplantation ◽  
Epstein Barr Virus ◽  
Solid Organ Transplantation ◽  
Lymphoproliferative Disease ◽  
Solid Organ ◽  
Barr Virus ◽  
Posttransplant Lymphoproliferative Disease ◽  
Epstein Barr

Case 38

2020 ◽  
pp. 261-266
Author(s):  
Andrew Woodhouse
Keyword(s):  
B Cells ◽  
T Lymphocytes ◽  
Lymphoproliferative Disease ◽  
Solid Organ ◽  
Post Transplant ◽  
Barr Virus ◽  
Cd20 Antibody ◽  
Epstein Barr ◽  
Anti Cd20 ◽  
Lymphoid Proliferation

Post-transplant lymphoproliferative disease (PTLD) is a disorder of lymphoid proliferation seen in recipients of solid organ or haematopoietic transplants as a consequence of immunosuppression. A spectrum of disease is recognized ranging from non-malignant polyclonal proliferation of B cells to monoclonal proliferation of B or T lymphocytes which have features in common with lymphomas. Epstein–Barr virus (EBV) is associated with a majority of cases although it is not a universal feature. Treatment with anti-CD20 antibody in addition to reduction in immunosuppression has become the most common treatment approach.

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