Alterations in NKG2A and NKG2C Subsets of Natural Killer Cells Following Epstein–Barr Virus Reactivation in CTLA4Ig-based Haploidentical Transplantation Is Associated With Increased Chronic Graft-Versus-Host Disease
| Autor: | Sarita Rani Jaiswal, Prakash Bhakuni, Suparno Chakrabarti, Aditi Chakrabarti, Hema Malini Aiyar, Gitali Bhagwati |
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| Rok vydání: | 2020 |
| Předmět: |
Adult
Male Epstein-Barr Virus Infections Herpesvirus 4 Human Transplantation Conditioning Adolescent Cyclophosphamide Graft vs Host Disease chemical and pharmacologic phenomena Disease 030230 surgery medicine.disease_cause Virus Abatacept Young Adult 03 medical and health sciences 0302 clinical medicine hemic and lymphatic diseases medicine Humans Child Aged Transplantation Haploidentical transplantation business.industry Incidence Incidence (epidemiology) Hematopoietic Stem Cell Transplantation Middle Aged medicine.disease Epstein–Barr virus Blockade Killer Cells Natural surgical procedures operative Graft-versus-host disease Child Preschool Chronic Disease Transplantation Haploidentical Immunology Female Virus Activation 030211 gastroenterology & hepatology NK Cell Lectin-Like Receptor Subfamily C business Immunosuppressive Agents medicine.drug |
| Zdroj: | Transplantation. 104:e23-e30 |
| ISSN: | 0041-1337 |
| Popis: | BACKGROUND The impact of newer approaches to haploidentical transplantation on Epstein-Barr virus (EBV) is largely unknown. METHODS We prospectively evaluated the incidence of EBV reactivation and its impact on transplantation outcomes in 71 patients undergoing haploidentical transplantation with posttransplantation cyclophosphamide in combination with CTLA4Ig-based T-costimulation blockade. RESULTS Eight patients developed EBV reactivation at a median of 96 days with no incidence of lymphoproliferative disorder. There was no impact of EBV reactivation on acute graft-versus-host disease (GVHD), nonrelapse mortality, progression-free, or overall survival. Despite an overall incidence of 19%, there was a significant increase in chronic GVHD following EBV reactivation (62.5% versus 8%; P = 0.01). NKG2A subset of CD56 natural killer cells increased substantially and persisted following EBV reactivation and chronic GVHD, with a reciprocal decrease in NKG2C subset, whereas the reverse was witnessed in those without chronic GVHD (P < 0.01). Increase in NKG2C subset and a decrease in the NKG2A subset were witnessed within 3 months of subsidence of chronic GVHD. CONCLUSIONS Thus, CTLA4Ig-based haploidentical transplantation was associated with a low incidence of EBV reactivation without EBV-lymphoproliferative disorder. However, EBV reactivation was associated with a sustained alteration in NKG2A and NKG2C subsets of CD56 natural killer cells which might have a pathogenic role in chronic GVHD. |
| Databáze: | OpenAIRE |
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