Understanding the Immunopathology of HTLV-1-Associated Adult T-Cell Leukemia/Lymphoma: A Comprehensive Review

Human T-cell leukemia virus type-1 (HTLV-1) causes adult T-cell leukemia/lymphoma (ATL). HTLV-1 carriers have a lifelong asymptomatic balance between infected cells and host antiviral immunity; however, 5–10% of carriers lose this balance and develop ATL. Coinfection with <i>Strongyloides</...

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Main Authors: Shingo Nakahata, Daniel Enriquez-Vera, M. Ishrat Jahan, Kenji Sugata, Yorifumi Satou
Format: Article
Language:English
Published: MDPI AG 2023-10-01
Series:Biomolecules
Subjects:
Online Access:https://www.mdpi.com/2218-273X/13/10/1543
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author Shingo Nakahata
Daniel Enriquez-Vera
M. Ishrat Jahan
Kenji Sugata
Yorifumi Satou
author_facet Shingo Nakahata
Daniel Enriquez-Vera
M. Ishrat Jahan
Kenji Sugata
Yorifumi Satou
author_sort Shingo Nakahata
collection DOAJ
description Human T-cell leukemia virus type-1 (HTLV-1) causes adult T-cell leukemia/lymphoma (ATL). HTLV-1 carriers have a lifelong asymptomatic balance between infected cells and host antiviral immunity; however, 5–10% of carriers lose this balance and develop ATL. Coinfection with <i>Strongyloides</i> promotes ATL development, suggesting that the immunological status of infected individuals is a determinant of HTLV-1 pathogenicity. As CD4+ T cells play a central role in host immunity, the deregulation of their function and differentiation via HTLV-1 promotes the immune evasion of infected T cells. During ATL development, the accumulation of genetic and epigenetic alterations in key host immunity-related genes further disturbs the immunological balance. Various approaches are available for treating these abnormalities; however, hematopoietic stem cell transplantation is currently the only treatment with the potential to cure ATL. The patient’s immune state may contribute to the treatment outcome. Additionally, the activity of the anti-CC chemokine receptor 4 antibody, mogamulizumab, depends on immune function, including antibody-dependent cytotoxicity. In this comprehensive review, we summarize the immunopathogenesis of HTLV-1 infection in ATL and discuss the clinical findings that should be considered when developing treatment strategies for ATL.
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spelling doaj.art-f97c196f0a734d18a7d67724717264182023-11-19T15:50:44ZengMDPI AGBiomolecules2218-273X2023-10-011310154310.3390/biom13101543Understanding the Immunopathology of HTLV-1-Associated Adult T-Cell Leukemia/Lymphoma: A Comprehensive ReviewShingo Nakahata0Daniel Enriquez-Vera1M. Ishrat Jahan2Kenji Sugata3Yorifumi Satou4Division of HTLV-1/ATL Carcinogenesis and Therapeutics, Joint Research Center for Human Retrovirus Infection, Kagoshima University, Kagoshima 890-8544, JapanDivision of HTLV-1/ATL Carcinogenesis and Therapeutics, Joint Research Center for Human Retrovirus Infection, Kagoshima University, Kagoshima 890-8544, JapanDivision of Genomics and Transcriptomics, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto 860-8556, JapanDivision of Genomics and Transcriptomics, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto 860-8556, JapanDivision of Genomics and Transcriptomics, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto 860-8556, JapanHuman T-cell leukemia virus type-1 (HTLV-1) causes adult T-cell leukemia/lymphoma (ATL). HTLV-1 carriers have a lifelong asymptomatic balance between infected cells and host antiviral immunity; however, 5–10% of carriers lose this balance and develop ATL. Coinfection with <i>Strongyloides</i> promotes ATL development, suggesting that the immunological status of infected individuals is a determinant of HTLV-1 pathogenicity. As CD4+ T cells play a central role in host immunity, the deregulation of their function and differentiation via HTLV-1 promotes the immune evasion of infected T cells. During ATL development, the accumulation of genetic and epigenetic alterations in key host immunity-related genes further disturbs the immunological balance. Various approaches are available for treating these abnormalities; however, hematopoietic stem cell transplantation is currently the only treatment with the potential to cure ATL. The patient’s immune state may contribute to the treatment outcome. Additionally, the activity of the anti-CC chemokine receptor 4 antibody, mogamulizumab, depends on immune function, including antibody-dependent cytotoxicity. In this comprehensive review, we summarize the immunopathogenesis of HTLV-1 infection in ATL and discuss the clinical findings that should be considered when developing treatment strategies for ATL.https://www.mdpi.com/2218-273X/13/10/1543human T-cell leukemia virus type 1adult T-cell leukemia/lymphomaviral genesgenetic alterationsimmune responsehost–pathogen interaction
spellingShingle Shingo Nakahata
Daniel Enriquez-Vera
M. Ishrat Jahan
Kenji Sugata
Yorifumi Satou
Understanding the Immunopathology of HTLV-1-Associated Adult T-Cell Leukemia/Lymphoma: A Comprehensive Review
Biomolecules
human T-cell leukemia virus type 1
adult T-cell leukemia/lymphoma
viral genes
genetic alterations
immune response
host–pathogen interaction
title Understanding the Immunopathology of HTLV-1-Associated Adult T-Cell Leukemia/Lymphoma: A Comprehensive Review
title_full Understanding the Immunopathology of HTLV-1-Associated Adult T-Cell Leukemia/Lymphoma: A Comprehensive Review
title_fullStr Understanding the Immunopathology of HTLV-1-Associated Adult T-Cell Leukemia/Lymphoma: A Comprehensive Review
title_full_unstemmed Understanding the Immunopathology of HTLV-1-Associated Adult T-Cell Leukemia/Lymphoma: A Comprehensive Review
title_short Understanding the Immunopathology of HTLV-1-Associated Adult T-Cell Leukemia/Lymphoma: A Comprehensive Review
title_sort understanding the immunopathology of htlv 1 associated adult t cell leukemia lymphoma a comprehensive review
topic human T-cell leukemia virus type 1
adult T-cell leukemia/lymphoma
viral genes
genetic alterations
immune response
host–pathogen interaction
url https://www.mdpi.com/2218-273X/13/10/1543
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