NDLI: Mediators of central nervous system damage during the progression of human T-cell leukemia type I-associated myelopathy/tropical spastic paraparesis

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Journal of NeuroVirology : Volume 9, Issue 4, July 2003

Journal of NeuroVirology : Volume 9, Issue 3, May 2003

Journal of NeuroVirology : Volume 9, Issue 2, March 2003

Journal of NeuroVirology : Volume 9, Issue 1, Supplement,January 2003

Journal of NeuroVirology : Volume 9, Issue 1, January 2003

Journal of NeuroVirology : Volume 8

Journal of NeuroVirology : Volume 7

Mediators of central nervous system damage during the progression of human T-cell leukemia type I-associated myelopathy/tropical spastic paraparesis

Content Provider	Springer Nature Link
Author	Barmak, Kate Harhaj, Edward W. Wigdahl, Brian
Copyright Year	2003
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.
Starting Page	522
Ending Page	529
Page Count	8
File Format	PDF
ISSN	13550284
Journal	Journal of NeuroVirology
Volume Number	9
Issue Number	5
e-ISSN	15382443
Language	English
Publisher	Springer-Verlag
Publisher Date	2003-01-01
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	blood-brain barrier CD8$^{+}$ T cells cerebrospinal fluid CTLs dendritic cells HAM/TSP HTLV-I molecular mimickry neurologic disease retrovirus Tax Neurosciences Virology Infectious Diseases Immunology Neurology
Content Type	Text
Resource Type	Article
Subject	Neurology Virology Neurology (clinical) Cellular and Molecular Neuroscience

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Selected cytotoxic T lymphocytes with high specificity for HTLV-I in cerebrospinal fluid from a HAM/TSP patient

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Mediators of central nervous system damage during the progression of human T-cell leukemia type I-associated myelopathy/tropical spastic paraparesis

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Mediators of central nervous system damage during the progression of human T-cell leukemia type I-associated myelopathy/tropical spastic paraparesis