HTLV-I alters the multidrug resistance associated protein 1 (ABCC1/MRP1) expression and activity in human T cells

Abstract The human T cell lymphotropic/leukaemia virus type I (HTLV-I) causes HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP). The multidrug resistance associated protein 1 (ABCC1) plays multiple functions in physiopathologic responses. The expression and activity of ABCC1 was st...

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Published in:Journal of neuroimmunology 2007-04, Vol.185 (1), p.175-181
Main Authors: Echevarria-Lima, Juliana, Rumjanek, Vivian M, Kyle-Cezar, Fernanda, Harab, Ramza C, Leite, Ana Claudia Celestino B, dos Santos Ornellas, Débora, Moralles, Marcelo Marcos, Araújo, Abelardo Q.C, Andrada-Serpa, Maria José
Format: Article
Language:English
Subjects:
ABCC 1
Adult
Aged
Allergy and Immunology
Asymptomatic carriers
Blotting, Western
CD4-Positive T-Lymphocytes - metabolism
CD4-Positive T-Lymphocytes - virology
CD8-Positive T-Lymphocytes - metabolism
CD8-Positive T-Lymphocytes - virology
Female
Flow Cytometry
HAM/TSP
HTLV-I
HTLV-I Infections - metabolism
Human T-lymphotropic virus 1
Humans
Male
Middle Aged
Multidrug Resistance-Associated Proteins - biosynthesis
Neurology
Paraparesis, Tropical Spastic - metabolism
Reverse Transcriptase Polymerase Chain Reaction
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Summary:Abstract The human T cell lymphotropic/leukaemia virus type I (HTLV-I) causes HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP). The multidrug resistance associated protein 1 (ABCC1) plays multiple functions in physiopathologic responses. The expression and activity of ABCC1 was studied in T lymphocytes from uninfected and HTLV-I-infected individuals (both asymptomatic and symptomatic/HAM/TSP). ABCC1 expression and activity was reduced to nearly half in T lymphocytes from infected patients compared to control lymphocytes. Only 51.6% of CD4+ cells from HAM/TSP patients expressed ABCC1 whereas this was seen in 60.3% from asymptomatic individuals, compared to an expression of around 86% in controls. Our results suggest that ABCC1 is negatively regulated in HTVL-I infection, supplying a novel target to investigate the pathogenesis of HTLV-I.
ISSN:0165-5728
1872-8421
DOI:10.1016/j.jneuroim.2007.01.008