Exaggerated Messenger RNA Expression of Inflammatory Cytokines in Human T-Cell Lymphotropic Virus Type I--Associated Myelopathy

Different Cytokine Production in Tax‐Expressing Cells between Patients with Human T Cell Lymphotropic Virus Type I (HTLV‐I)–Associated Myelopathy/Tropical Spastic Paraparesis and Asymptomatic HTLV‐I Carriers

“…In addition, the HTLV-I provirus load may influence cytokine production, because HTLV-I-infected cells possibly produce greater amounts of cytokines, compared with uninfected cells, through the transactivational activity of Tax on cytokine genes. However, previous studies have not made it clear whether the higher production of these cytokine mRNA in the PBMCs of patients with HAM/TSP versus ACs is simply caused by the higher HTLV-I provirus load or whether the cytokine expression in individual Tax-expressing cells is higher in patients with HAM/ TSP [11]. In addition, previous results regarding the cytokine production were obtained in the supernatant of PBMCs after 3-4 days of culture, and it was not determined whether this high cytokine production was produced in HTLV-I -infected cells themselves [12].…”

“…However, there are ACs with a high HTLV-I provirus load [8]; therefore, we wanted to determine whether there were factors other than HTLV-I provirus load that would influence the outcome of HTLV-I infection. Second, the production of inflammatory cytokines, such as interferon (IFN)-g and tumor necrosis factor (TNF)-a have been examined in patients with HAM/TSP [11][12][13], and an immunocytochemical study revealed overexpression of IFN-g and TNF-a by infiltrating lymphocytes in the central nervous system (CNS) of patients with HAM/TSP [14]. It also has been reported that the adhesion of lymphocytes to cultured cerebral endothelium was increased by IFN-g and/or TNF-a [15].…”

“…Furthermore, IFN-g induces major histocompatibility complex (MHC) class II antigens [16] and might elicit a T cell-mediated immune response leading to CNS damage [17], and inflammatory cytokines were postulated to play a role in the pathogenesis of HAM/TSP [18]. Expression of these cytokine genes, as determined by reverse-transcriptase polymerase chain reaction (RT-PCR), is detected more frequently in patients with HAM/TSP than in ACs or seronegative control subjects [11]. An increased production of these cytokines in patients with HAM/TSP was reported in the supernatant of cultured PBMCs, compared with that in uninfected healthy control subjects, as described elsewhere [12].…”

Different Cytokine Production in Tax‐Expressing Cells between Patients with Human T Cell Lymphotropic Virus Type I (HTLV‐I)–Associated Myelopathy/Tropical Spastic Paraparesis and Asymptomatic HTLV‐I Carriers

“…In addition, the HTLV-I provirus load may influence cytokine production, because HTLV-I-infected cells possibly produce greater amounts of cytokines, compared with uninfected cells, through the transactivational activity of Tax on cytokine genes. However, previous studies have not made it clear whether the higher production of these cytokine mRNA in the PBMCs of patients with HAM/TSP versus ACs is simply caused by the higher HTLV-I provirus load or whether the cytokine expression in individual Tax-expressing cells is higher in patients with HAM/ TSP [11]. In addition, previous results regarding the cytokine production were obtained in the supernatant of PBMCs after 3-4 days of culture, and it was not determined whether this high cytokine production was produced in HTLV-I -infected cells themselves [12].…”

“…However, there are ACs with a high HTLV-I provirus load [8]; therefore, we wanted to determine whether there were factors other than HTLV-I provirus load that would influence the outcome of HTLV-I infection. Second, the production of inflammatory cytokines, such as interferon (IFN)-g and tumor necrosis factor (TNF)-a have been examined in patients with HAM/TSP [11][12][13], and an immunocytochemical study revealed overexpression of IFN-g and TNF-a by infiltrating lymphocytes in the central nervous system (CNS) of patients with HAM/TSP [14]. It also has been reported that the adhesion of lymphocytes to cultured cerebral endothelium was increased by IFN-g and/or TNF-a [15].…”

“…Furthermore, IFN-g induces major histocompatibility complex (MHC) class II antigens [16] and might elicit a T cell-mediated immune response leading to CNS damage [17], and inflammatory cytokines were postulated to play a role in the pathogenesis of HAM/TSP [18]. Expression of these cytokine genes, as determined by reverse-transcriptase polymerase chain reaction (RT-PCR), is detected more frequently in patients with HAM/TSP than in ACs or seronegative control subjects [11]. An increased production of these cytokines in patients with HAM/TSP was reported in the supernatant of cultured PBMCs, compared with that in uninfected healthy control subjects, as described elsewhere [12].…”

Inhibition of immune activation by a novel nuclear factor-kappa B inhibitor in HTLV-I–associated neurologic disease

“…21 STAT proteins function to mediate cytokine signal transduction, such that the detection of STAT activation can be used as an indicator of cytokine production and signaling. 22 We analyzed the activation of STAT5 protein to examine the induction of cytokines in PBMCs from subjects with HAM/TSP.…”

Neuroimmunity of HTLV-I Infection

“…It has been reported that CD4+ cells in HAM/TSP patients deviate to Th1-like phenotype as characterized by upregulated secretion of proinflammatory cytokines such as IFN-g, TNF-a, and IL-2 and downregulation of Th 2 cytokines such as IL-4 (Watanabe et al 1995; Nakamura et al 2000; Horiuchi et al 2000; Hanon et al 2001; Goon et al 2003). Th1 cells but not Th2 cells are reported to bind to P- and E-selectin expressed on endothelial cells (Austrup et al 1997).…”

Different Cytokine Production in Tax‐Expressing Cells between Patients with Human T Cell Lymphotropic Virus Type I (HTLV‐I)–Associated Myelopathy/Tropical Spastic Paraparesis and Asymptomatic HTLV‐I Carriers

“…In addition, the HTLV-I provirus load may influence cytokine production, because HTLV-I-infected cells possibly produce greater amounts of cytokines, compared with uninfected cells, through the transactivational activity of Tax on cytokine genes. However, previous studies have not made it clear whether the higher production of these cytokine mRNA in the PBMCs of patients with HAM/TSP versus ACs is simply caused by the higher HTLV-I provirus load or whether the cytokine expression in individual Tax-expressing cells is higher in patients with HAM/ TSP [11]. In addition, previous results regarding the cytokine production were obtained in the supernatant of PBMCs after 3-4 days of culture, and it was not determined whether this high cytokine production was produced in HTLV-I -infected cells themselves [12].…”

“…However, there are ACs with a high HTLV-I provirus load [8]; therefore, we wanted to determine whether there were factors other than HTLV-I provirus load that would influence the outcome of HTLV-I infection. Second, the production of inflammatory cytokines, such as interferon (IFN)-g and tumor necrosis factor (TNF)-a have been examined in patients with HAM/TSP [11][12][13], and an immunocytochemical study revealed overexpression of IFN-g and TNF-a by infiltrating lymphocytes in the central nervous system (CNS) of patients with HAM/TSP [14]. It also has been reported that the adhesion of lymphocytes to cultured cerebral endothelium was increased by IFN-g and/or TNF-a [15].…”

“…Furthermore, IFN-g induces major histocompatibility complex (MHC) class II antigens [16] and might elicit a T cell-mediated immune response leading to CNS damage [17], and inflammatory cytokines were postulated to play a role in the pathogenesis of HAM/TSP [18]. Expression of these cytokine genes, as determined by reverse-transcriptase polymerase chain reaction (RT-PCR), is detected more frequently in patients with HAM/TSP than in ACs or seronegative control subjects [11]. An increased production of these cytokines in patients with HAM/TSP was reported in the supernatant of cultured PBMCs, compared with that in uninfected healthy control subjects, as described elsewhere [12].…”

Inhibition of immune activation by a novel nuclear factor-kappa B inhibitor in HTLV-I–associated neurologic disease

“…21 STAT proteins function to mediate cytokine signal transduction, such that the detection of STAT activation can be used as an indicator of cytokine production and signaling. 22 We analyzed the activation of STAT5 protein to examine the induction of cytokines in PBMCs from subjects with HAM/TSP.…”

Neuroimmunity of HTLV-I Infection

“…It has been reported that CD4+ cells in HAM/TSP patients deviate to Th1-like phenotype as characterized by upregulated secretion of proinflammatory cytokines such as IFN-g, TNF-a, and IL-2 and downregulation of Th 2 cytokines such as IL-4 (Watanabe et al 1995; Nakamura et al 2000; Horiuchi et al 2000; Hanon et al 2001; Goon et al 2003). Th1 cells but not Th2 cells are reported to bind to P- and E-selectin expressed on endothelial cells (Austrup et al 1997).…”

Different Cytokine Production in Tax‐Expressing Cells between Patients with Human T Cell Lymphotropic Virus Type I (HTLV‐I)–Associated Myelopathy/Tropical Spastic Paraparesis and Asymptomatic HTLV‐I Carriers

“…In addition, the HTLV-I provirus load may influence cytokine production, because HTLV-I-infected cells possibly produce greater amounts of cytokines, compared with uninfected cells, through the transactivational activity of Tax on cytokine genes. However, previous studies have not made it clear whether the higher production of these cytokine mRNA in the PBMCs of patients with HAM/TSP versus ACs is simply caused by the higher HTLV-I provirus load or whether the cytokine expression in individual Tax-expressing cells is higher in patients with HAM/ TSP [11]. In addition, previous results regarding the cytokine production were obtained in the supernatant of PBMCs after 3-4 days of culture, and it was not determined whether this high cytokine production was produced in HTLV-I -infected cells themselves [12].…”

“…However, there are ACs with a high HTLV-I provirus load [8]; therefore, we wanted to determine whether there were factors other than HTLV-I provirus load that would influence the outcome of HTLV-I infection. Second, the production of inflammatory cytokines, such as interferon (IFN)-g and tumor necrosis factor (TNF)-a have been examined in patients with HAM/TSP [11][12][13], and an immunocytochemical study revealed overexpression of IFN-g and TNF-a by infiltrating lymphocytes in the central nervous system (CNS) of patients with HAM/TSP [14]. It also has been reported that the adhesion of lymphocytes to cultured cerebral endothelium was increased by IFN-g and/or TNF-a [15].…”

“…Furthermore, IFN-g induces major histocompatibility complex (MHC) class II antigens [16] and might elicit a T cell-mediated immune response leading to CNS damage [17], and inflammatory cytokines were postulated to play a role in the pathogenesis of HAM/TSP [18]. Expression of these cytokine genes, as determined by reverse-transcriptase polymerase chain reaction (RT-PCR), is detected more frequently in patients with HAM/TSP than in ACs or seronegative control subjects [11]. An increased production of these cytokines in patients with HAM/TSP was reported in the supernatant of cultured PBMCs, compared with that in uninfected healthy control subjects, as described elsewhere [12].…”

Inhibition of immune activation by a novel nuclear factor-kappa B inhibitor in HTLV-I–associated neurologic disease

“…21 STAT proteins function to mediate cytokine signal transduction, such that the detection of STAT activation can be used as an indicator of cytokine production and signaling. 22 We analyzed the activation of STAT5 protein to examine the induction of cytokines in PBMCs from subjects with HAM/TSP.…”

Neuroimmunity of HTLV-I Infection

“…It has been reported that CD4+ cells in HAM/TSP patients deviate to Th1-like phenotype as characterized by upregulated secretion of proinflammatory cytokines such as IFN-g, TNF-a, and IL-2 and downregulation of Th 2 cytokines such as IL-4 (Watanabe et al 1995; Nakamura et al 2000; Horiuchi et al 2000; Hanon et al 2001; Goon et al 2003). Th1 cells but not Th2 cells are reported to bind to P- and E-selectin expressed on endothelial cells (Austrup et al 1997).…”