Leukaemia of novel gastrointestinal T-lymphocyte population infected with HTLV-I

Hattori, Toshio; Asou, Norio; Suzushima, Hitoshi; Takatsuki, Kiyoshi; Tanaka, Keiko; Naito, Katsusuke; Natori, H; Ōizumi, Kōtaro

doi:10.1016/0140-6736(91)90737-a

Cited by 25 publications

(8 citation statements)

References 9 publications

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“…Shimoyama proposed criteria for the diagnosis of the various clinical forms in 19913; they are summarised in box 1. Usually the disease is disseminated, although lymphomas confined to the gut and central nervous system have been recognised 4 – 6. The outlook of ATLL is poor as most patients do not respond or have short-lived partial responses to treatments used in other T-cell lymphomas.…”

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confidence: 99%

Adult T-cell leukaemia/lymphoma

2007

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Adult T-cell leukaemia/lymphoma (ATLL) is a mature T-cell neoplasm of post-thymic lymphocytes aetiologically linked to the human T-cell lymphotropic virus, HTLV-I, and with a distinct geographical distribution. The disease manifests with leukaemia in greater than two thirds of patients, while the remaining patients have a lymphomatous form. According to the disease manifestations, various forms which differ in clinical course and prognosis have been recognised: acute, chronic, smouldering and lymphoma. Organomegaly, skin involvement, circulating atypical lymphocytes ("flower" cells) with a CD4+ CD25+ phenotype and hypercalcaemia are the most common disease features. The diagnosis should be based on a constellation of clinical features and laboratory investigations. The latter comprise: lymphocyte morphology, immunophenotype, histology of the tissues affected in the pure lymphoma forms and serology or DNA analysis for HTLV-I. The differential diagnosis of ATLL includes other mature T-cell neoplasms such as T-cell prolymphocytic leukaemia (T-PLL), Sézary syndrome (SS), peripheral T-cell lymphomas and occasionally healthy carriers of the virus or Hodgkin disease. The clinical course is aggressive with a median survival of less than 12 months in the acute and lymphoma forms. Despite major advances in understanding the pathogenesis of the disease, management of these patients remains a challenge for clinicians as they do not respond or achieve only transient responses to therapies used in high-grade lymphomas. The use of antiretroviral agents such as zidovudine in combination with interferon-alpha, with or without concomitant chemotherapy, has shown activity in this disease with improvement in survival and response rate. Consolidation with high dose therapy and autologous or allogeneic stem-cell transplantation should be considered in young patients.

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Adult T-cell leukaemia/lymphoma

2007

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“…ATL/ATLL cells were initially shown to be positive for mature T-cell surface antigens CD3, CD4, and CD25, and negative for CD8 with rare occasions of double negativity or double positivity for CD4 and CD8 (Hattori et al 1981;Hattori et al 1991). Subsequent studies on the nature of ATL/ATLL cells have shown that they are also positive for regulatory T-cell (Treg) markers, such as FoxP3 (Karube et al 2004;Roncador et al 2005) and the CC chemokine receptor 4 (CCR4) (Yoshie et al 2002).…”

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confidence: 99%

Galectin-9 as a Predictive Marker for the Onset of Immune-Related Adverse Effects Associated with Anti-CCR4 MoAb Therapy in Patients with Adult T Cell Leukemia

Mohammed

Chagan-Yasutan

Ashino

et al. 2017

Tohoku J. Exp. Med.

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Adult T-cell leukemia/lymphoma (ATL/ATLL) is one of the most malignant lymphomas with poor prognosis. ATL/ATLL cells express CC chemokine receptor 4, and mogamulizumab (anti-CCR4 monoclonal antibody) exhibits strong cytotoxicity for ATL/ATLL cells. We analyzed plasma samples of 6 patients with ATL/ATLL treated with chemotherapy followed by mogamulizumab therapy (mogatherapy) for changes in the levels of biomarkers in relation to immune-related adverse effects. As treatment is often associated with skin eruptions, we investigated the profiles of inflammatory cytokines, including galectin-9 (Gal-9), which becomes increased in various infectious diseases and allergic patients. Gal-9, soluble interleukin (IL)-2 receptor, tumor necrosis factor-α, and IL-10 levels were increased before chemotherapy, and Gal-9 levels were associated with the sIL-2 receptor, which reflects tumor burden. Inflammatory levels decreased after chemotherapy. After mogatherapy, 5 of 6 patients attained complete remission (CR), whereas 1 patient showed no response (NR) and died. Among 5 patients with CR, the biomarkers remained low during mogatherapy, except for a 3-5-fold increment in Gal-9 (associated with skin eruptions). A skin biopsy showed infiltration by inflammatory cells and Gal-9 synthesis in areas with CD8 cell infiltration. In the patient with NR, increased levels of Gal-9 and the aforementioned biomarkers were noted 3 days after mogatherapy, followed by opportunistic infections resembling immune reconstitution inflammatory syndrome. Therefore, an increased Gal-9 plasma level in ATL/ATLL indicates tumor burden and reflects immune activation by mogatherapy. These findings may indicate that an increase in the Gal-9 level, a novel immune checkpoint molecule, can reflect immune-related adverse effects of various biotherapies.

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“…They represent a small subpopulation of peripheral blood lymphocytes (PBL) in most healthy adults but are increased in some patients with systemic and cutaneous autoimmune disorders (17)(18)(19), in children suffering from certain genetic immunodeficiency syndromes (20,21), in some individuals infected with T-cell leukemia virus type I or human immunodeficiency virus (22,23), and in some apparently healthy individuals (24) (37). mAbs were anti-Leu-4 (CD3), anti-Leu-3 (CD4), anti-Leu-2a (CD8), anti-Leu-15 (CD11b), anti-Leu-llc (CD16), antiinterleukin-2 receptor (CD25, p55), anti-Leu-19 (CD56), and antiLeu-7 (CD57), anti-TCR-1 (TCR a/(3), anti-TCRy/8-1 (TCRCy), anti-Leu-8 (L-selectin), and anti-HLA-DR, all purchased from Becton Dickinson, and 2H4 (CD45RA) from Coulter (Raritan, NJ) and UCHL1 (CD45RO) from Dako.…”

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Human T-cell receptor (TCR) alpha/beta + CD4-CD8- T cells express oligoclonal TCRs, share junctional motifs across TCR V beta-gene families, and phenotypically resemble memory T cells.

Brooks

Balk

Aupeix

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

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Most human T cells express the TCR a/Il and either CD4 or CD8 molecules (single positive, SP); however, small numbers lack CD4 and CD8. In inbred mice, a/,B CD4-CD8-(double negative, DN) T cells preferentially express certain 13 variable region (Vp) marrow a//3 T cells also lack CD4 and CD8 and express a skewed TCR repertoire with preferential usage of Vp2 and limited junctional diversity (12). These findings have suggested that a/fl DN T cells may be subject to thymic and/or extrathymic selection pressures distinct from those generating a/fl SP T cells. Therefore, the physiologic potential of a/fl DN T cells as well as the ligands they recognize may also be unique. This has been supported by the isolation of human a/fl DN T cell clones, which lyse target cells through recognition ofthe nonpolymorphic MHC-like CD1 molecules (13).In humans, a/fl DN T cells have been identified in peripheral blood, thymus, and skin (14-16). They represent a small subpopulation of peripheral blood lymphocytes (PBL) in most healthy adults but are increased in some patients with systemic and cutaneous autoimmune disorders (17)(18)(19)

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Leukaemia of novel gastrointestinal T-lymphocyte population infected with HTLV-I

Cited by 25 publications

References 9 publications

Adult T-cell leukaemia/lymphoma

Adult T-cell leukaemia/lymphoma

Galectin-9 as a Predictive Marker for the Onset of Immune-Related Adverse Effects Associated with Anti-CCR4 MoAb Therapy in Patients with Adult T Cell Leukemia

Human T-cell receptor (TCR) alpha/beta + CD4-CD8- T cells express oligoclonal TCRs, share junctional motifs across TCR V beta-gene families, and phenotypically resemble memory T cells.

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