Journal article
Mediators of central nervous system damage during the progression of human T-cell leukemia type I-associated myelopathy/tropical spastic paraparesis
Journal of neurovirology, v 9(5), pp 522-529
Sep 2003
PMID: 13129766
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
Human T-cell leukemia virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) represents one of the most devastating diseases associated with HTLV-I infection. Despite the delineation of clinical features associated with this neurologic disease, more progress needs to be made with respect to understanding the molecular mechanisms relating to the genesis of HAM/TSP. Several factors have been hypothesized to contribute to whether an HTLV-I-infected individual remains asymptomatic, develops adult T-cell leukemia (ATL), or progresses to HAM/TSP. Among the most intriguing of these factors is the immune response mounted by the host against HTLV-I. Several cell populations are crucial with respect to generating an efficient immune response against the virus. This includes CD4+ T cells, CD8+ T cells, dendritic cells (DCs), monocytes/macrophages, and HTLV-I-infected cells that interact with immune cells to stimulate their effector functions. Although all of these cell types likely play important roles in the etiology of HAM/TSP, this review focuses specifically on the potential function of the CD8+ T-cell population during the progression of HTLV-I-induced neurologic disease. The immune response in HAM/TSP patients may transition from a beneficial response aimed at controlling the viral infection, to a detrimental response that ultimately participates in mediating the pathology observed in HAM/TSP. In this respect, the generation of a hyperactive CD8+ cytotoxic T lymphocyte (CTL) response primarily targeting the HTLV-I Tax protein likely plays a key role in the genesis of pathologic abnormalities associated with HAM/TSP. The efficiency and activity of Tax-specific CD8+ CTLs may be regulated at a number of levels, and deregulation of Tax-specific CTL activation may contribute to HAM/TSP. This review focuses on potential mechanisms of central nervous system (CNS) damage associated with the genesis of HAM/TSP following HTLV-I infection, focusing on the role of the Tax-specific CTL compartment.
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Details
- Title
- Mediators of central nervous system damage during the progression of human T-cell leukemia type I-associated myelopathy/tropical spastic paraparesis
- Creators
- Kate Barmak - Laboratory for Molecular Retrovirology and Viral Neuropathogenesis, Department of Microbiology and Immunology The Pennsylvania State University, College of Medicine Hershey Pennsylvania USAEdward Harhaj - Laboratory for Molecular Retrovirology and Viral Neuropathogenesis, Department of Microbiology and Immunology The Pennsylvania State University, College of Medicine Hershey Pennsylvania USABrian Wigdahl - Department of Microbiology and Immunology (H107) Penn State College of Medicine 500 University Drive P.O. Box 850 17033 Hershey PA USA
- Publication Details
- Journal of neurovirology, v 9(5), pp 522-529
- Publisher
- Springer-Verlag; New York
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Microbiology and Immunology
- Web of Science ID
- WOS:000185334700002
- Scopus ID
- 2-s2.0-0142106300
- Other Identifier
- 991014878029104721
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- Web of Science research areas
- Neurosciences
- Virology