Cytotoxic and suppressor activities in patients with HTLV-I-associated myelopathy

Usuku, Koichiro; Nishizawa, Masatoyo; Osame, Mitsuhiro; Tabira, Takeshi

doi:10.1016/0165-5728(91)90107-i

Cited by 3 publications

(1 citation statement)

References 30 publications

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“…1995). Certain HLA haplotypes have been associated with the development of TSP/HAM, which is not the case for ATL (Usuku et al . 1991; Jeffery et al .…”

Section: Htlv‐1‐associated Diseasesmentioning

confidence: 99%

Molecular biology and pathogenesis of the human T‐cell leukaemia/lymphotropic virus Type‐1 (HTLV‐1)

Johnson

Harrod

Franchini

2001

Int J Experimental Path

103

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Retroviruses are associated with a variety of diseases, including immunological and neurological disorders, and various forms of cancer. In humans, the Human T-cell Leukaemia/Lymphotropic virus type 1 (HTLV-1), which belongs to the Oncovirus family, is the aetiological agent of two diverse diseases: Adult T-cell leukaemia/lymphoma (ATLL) (Poiesz et al. 1980; Hinuma et al. 1981; Yoshida et al. 1982), as well as the neurological disorder tropical spastic paraparesis/HTLV-1-associated myelopathy (TSP/HAM) (Gessain et al. 1985; Rodgers-Johnson et al. 1985; Osame et al. 1986). HTLV-1 is the only human retrovirus known to be the aetiological agent of cancer. A genetically related virus, HTLV-2, has been identified and isolated (Kalyanaraman et al. 1982). However, there has been no demonstration of a definitive aetiological role for HTLV-2 in human disease to date. Simian T-cell lymphotropic viruses types 1 and 2 (STLV-1 and -2) and bovine leukaemia virus (BLV) have also been classified in same group, Oncoviridae, based upon their similarities in genetic sequence and structure to HTLV-1 and -2 (Burny et al. 1988; Dekaban et al. 1995; Slattery et al. 1999). This article will focus on HTLV-1, reviewing its discovery, molecular biology, and its role in disease pathogenesis.

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“…1995). Certain HLA haplotypes have been associated with the development of TSP/HAM, which is not the case for ATL (Usuku et al . 1991; Jeffery et al .…”

Section: Htlv‐1‐associated Diseasesmentioning

confidence: 99%

Molecular biology and pathogenesis of the human T‐cell leukaemia/lymphotropic virus Type‐1 (HTLV‐1)

Johnson

Harrod

Franchini

2001

Int J Experimental Path

103

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Suppression of lymphocyte spontaneous proliferative response by proteolipid protein peptide in patients with HAM/TSP

et al. 1994

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To understand the immune mechanism suggested in HTLV-I-associated myelopathy (HAM/TSP), we investigated T cell response to proteolipid protein (PLP). Because of high autologous proliferative response (APR) of peripheral blood mononuclear cells (PBMC) in culture, the lymphocyte proliferation assay was not useful in this disease. Unexpectedly, however, APR was profoundly (70-98%) suppressed in 6 of 9 cases when PLP peptide 105-124 was added in the culture. PLP peptide 85-104 or 145-159 also suppressed APR in a few cases. Time course study showed that the peptide-mediated suppression became apparent after day 4 in culture. The results can be interpreted as that suppressor cells recognizing the PLP peptides were present in the PBMC of HAM/TSP patients and suppressed the APR as the consequence of antigen specific response. This may indicate that a T cell response to certain PLP determinants is involved in the pathomechanism of HAM/TSP at least in part. Molecular mimicry between PLP and HTLV-I may account for the T cell sensitization to PLP in HAM/TSP.

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Human T-cell lymphotropic virus type-I associated myelopathy complicated by optic neuritis.

Komaba

Kitamura

Terashi

et al. 1996

Journal of Nippon Medical School

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A 48-year-old Japanese woman from Kyushu was admitted to the Nippon Medical School First Hospital with complaints of numbness in both legs, gait disturbance, and urinary problems. On examination, her lower extremities were spastic with increased reflexes and positive Babinski sign. Sensation was absent below the T4 spinal level. The cerebrospinal fluid contained HTLV-I antibodies and she was diagnosed with HTLV-I associated myelopathy. Her symptoms were resolved with prednisolone, but six months later a visual disturbance of the left eye edema developed. Orbital CT scans showed that left optic nerve was edematous. T2 enhanced MRI revealed a high intensity lesion of the left optic nerve. ERG was normal and no VEP was detected in response to flashing stimulation to the left eye. The HTLV-I antigen titer of CBF was very high. Her optic neuritis improved following oral administration of prednisolone and retrobulbar injections of dexamethasone. This is the first case report of HTLV-I associated myelopathy complicated by optic neuritis.

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Cytotoxic and suppressor activities in patients with HTLV-I-associated myelopathy

Cited by 3 publications

References 30 publications

Molecular biology and pathogenesis of the human T‐cell leukaemia/lymphotropic virus Type‐1 (HTLV‐1)

Molecular biology and pathogenesis of the human T‐cell leukaemia/lymphotropic virus Type‐1 (HTLV‐1)

Suppression of lymphocyte spontaneous proliferative response by proteolipid protein peptide in patients with HAM/TSP

Human T-cell lymphotropic virus type-I associated myelopathy complicated by optic neuritis.

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