title: Th1/Th2 balance and HTLV-I proviral load in HAM/TSP patients treated with interferon-alpha.
abstract: We studied the immunological and virological effects of interferon-alpha (IFN-alpha) therapy in nine patients with HTLV-I-associated myelopathy (HAM/TSP). After therapy, the percentages of CCR5+ cells in CD4+ cells significantly decreased in the cerebrospinal fluid as well as blood. The therapy also significantly lowered the intracellular IFN-gamma+/interleukin-4+ T-cell ratio in blood. Those helper T-cell type 1 (Th1)-related responses tended to be higher and reduce more evidently following therapy in three patients who clinically improved. Also, all the three patients had one or more HTLV-I copies in five blood mononuclear cells. These results suggest that IFN-alpha suppresses Th1 responses in HAM/TSP and that the patients with higher Th1 immunity and proviral loads may be responders of the therapy. Larger-scale studies are needed to confirm the findings.
authors.affiliation: Department of Neurology, Tohoku University School of Medicine 1-1 Seiryomachi, Aobaku, Sendai 980-8574, Japan.
authors.forename: Juan
authors.initials: J
authors.lastname: Feng
authors.forename: Tatsuro
authors.initials: T
authors.lastname: Misu
authors.forename: Kazuo
authors.initials: K
authors.lastname: Fujihara
authors.forename: Naoko
authors.initials: N
authors.lastname: Misawa
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Koyanagi
authors.forename: Yusei
authors.initials: Y
authors.lastname: Shiga
authors.forename: Atsushi
authors.initials: A
authors.lastname: Takeda
authors.forename: Shigeru
authors.initials: S
authors.lastname: Sato
authors.forename: Sadao
authors.initials: S
authors.lastname: Takase
authors.forename: Takeshi
authors.initials: T
authors.lastname: Kohnosu
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Saito
authors.forename: Yasuto
authors.initials: Y
authors.lastname: Itoyama
mesh_terms: D000368:Aged; D000998:Antiviral Agents / Q000627:therapeutic use*; D004351:Drug Resistance / Q000276:immunology; D005260:Female; D005434:Flow Cytometry; D015368:Human T-lymphotropic virus 1 / Q000276:immunology*; D006801:Humans; D016898:Interferon-alpha / Q000627:therapeutic use*; D007371:Interferon-gamma / Q000096:biosynthesis; D015847:Interleukin-4 / Q000096:biosynthesis; D007424:Intracellular Fluid / Q000737:chemistry; D008297:Male; D008875:Middle Aged; D015493:Paraparesis, Tropical Spastic / Q000188:drug therapy / Q000276:immunology*; D016133:Polymerase Chain Reaction; D011533:Proviruses / Q000276:immunology*; D054397:Receptors, CCR3; D019713:Receptors, CCR5 / Q000378:metabolism; D054367:Receptors, CXCR3; D019707:Receptors, Chemokine / Q000378:metabolism; D006377:T-Lymphocytes, Helper-Inducer / Q000187:drug effects* / Q000276:immunology; D018417:Th1 Cells / Q000187:drug effects / Q000276:immunology; D018418:Th2 Cells / Q000187:drug effects / Q000276:immunology; D019562:Viral Load
chemical_list: D000998:Antiviral Agents; C515350:CCR3 protein, human; C515187:CXCR3 protein, human; D016898:Interferon-alpha; D054397:Receptors, CCR3; D019713:Receptors, CCR5; D054367:Receptors, CXCR3; D019707:Receptors, Chemokine; D015847:Interleukin-4; D007371:Interferon-gamma