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T Amagasaki

Publications and source records attributed to T Amagasaki.

At least 37 records · Page 2Linked to original sources
PubMed1985

A lymphoproliferative disorder of T gamma cells with the phenotype of cytotoxic/suppressor T-cell.

A 25-yr-old Japanese male showed unique T gamma cell proliferation different from cases reported previously. His clinical and hematological features were characterized by persistent high fever and the appearance of large lymphocytes with abundant cytoplasm and azurophilic granules in the peripheral blood (11% of the leukocyte differential count) and the ascitic fluid. These lymphocytes showed the ability to bind the Fc portion of IgG and they beared the antigen of cytotoxic/suppressor T-cell defined by monoclonal antibodies. T-cells from this patient suppressed the immunoglobulin production of normal B-cells by pokeweed mitogen, although a polyclonal hypergammaglobulinemia was observed in the serum. Chromosomal abnormality indicated the malignant nature of the proliferating T gamma cells in this patient. The clinical, hematological, and immunological findings characterized the disease of this patient as a distinct entity among the lymphoproliferative disorders of T-cell origin.

Adult↗
PubMed1985

T lymphomas associated with human T-cell leukemia-lymphoma virus may show phenotypic and functional differences from adult T-cell leukemias.

We report phenotypic and functional characterization of lymph node cells from 27 patients with T lymphoma from the Nagasaki district of Japan. Nagasaki is one of several areas where adult T-cell leukemia is endemic, and sera from 18 of 23 patients examined (78.3%) were positive for antibody to adult T-cell leukemia-associated antigen. The majority of cases (24 of 27) showed the Leu-2a-, 3a+, MASO36c- phenotype similar to adult T-cell leukemia, but seemed to be subdivided into four groups according to the presence or absence of Leu-1 antigen and the receptor for sheep erythrocytes (SRBC). Eleven cases had both Leu-1 antigen and the receptor for SRBC (E-RFC+, Leu-1+, 2a-, 3a+), but 6 cases lacked Leu-1 antigen (E-RFC+, Leu-1-, 2a-, 3a+), 4 cases lacked receptors for SRBC (E-RFC-, Leu-1+, 2a-, 3a+), and 3 cases lacked both of these markers (E-RFC-, Leu-1-, 2a-, 3a+). The effects of lymph node T cells on pokeweed mitogen (PWM)-induced normal B-cell differentiation was studied in 10 cases. Lymph node T cells of 5 cases showed helper activity without any suppressor activity, and 2 cases showed suppressor activity with almost no detectable helper activity, similar to adult T-cell leukemia cells. Two other cases lacked particular functional effects. These results suggest the possibility that Leu-3a+ T-cell lymphoma may be functionally subdivided into at least two types, a helper type and a suppressor (adult T-cell leukemia) type.

Adolescent↗
PubMed1985

Adult T cell leukemia with atypical surface phenotypes: clinical correlation.

The leukemic cells of 57 patients with adult T cell leukemia (ATL) were analyzed for their immunologic surface markers. Forty-four cases showed normal mature inducer/helper T cell phenotype (typical group: E-RFC+, Leu-1+, 2a-, 3a+ MASO36c-), but the other 13 cases showed unusual surface phenotypes (variant group) and could be subdivided into several groups (V1 to V5). Four cases had absent or low Leu-1 positivity (V1: E-RFC+, Leu-1-, 2a-, 3a+, MASO36c-), while two other cases with low Leu-1 positivity had both Leu-2a and 3a, a characteristic of cortical thymocytes, but were unreactive with MASO36c (V2: E-RFC+, Leu-1-, 2a+, 3a+, MASO36c-). Three cases lacked both Leu-2a and 3a despite having other T cell markers (V3: E-RFC+, Leu-1+, 2a-, 3a-, MASO36c-). The next three cases had low rosette-forming ability with sheep RBCs (V4: E-RFC-, Leu-1- approximately +, 2a- approximately +, 3a+, MASO36c-). Interestingly, one other case showed high reactivity against anti-Leu-7, which is believed to be one of the monoclonal antibodies directed against natural killer cells (V5: E-RFC+, Leu-1+, 2a-, 3a+, 7+, MASO36c-). Clinical and hematologic differences between the typical group and variant group were investigated, and it was found that the variant group (excluding V5) have statistically significant (P less than .002) higher serum lactic dehydrogenase (LDH) activity. The overall survival in the variant group was worse than in the typical group, but it was not quite statistically significant (P = .072). The median survival time was eight months for typical cases and only four months for variant cases; six cases died within two months. The V5 case was unusual not only because the patient's leukemic cells have Leu-7 antigen but also because she survived more than nine years after initial diagnosis. There seems to be some correlation between phenotypic diversity of ATL cells and prognosis.

Adult↗
PubMed1985

Preleukemic state of adult T cell leukemia: abnormal T lymphocytosis induced by human adult T cell leukemia-lymphoma virus.

We report the clinical, hematologic, and immunologic features of 18 preleukemic adult T cell leukemia (pre-ATL) cases with abnormal T lymphocytosis induced by human adult T cell leukemia-lymphoma virus (HTLV/ATLV). The patients were from the Nagasaki district, which is one of the most endemic areas of ATL in Japan. Pre-ATL is a subclinical T cell abnormality differing from ATL. It is characterized by an insidious onset and appearance of abnormal T lymphocytes (10% to 40%) in the peripheral blood without clinical symptoms except for a few cases transiently presenting fever, skin eruptions, and slight lymphadenopathies. Most abnormal T lymphocytes were small and mature with incised or lobulated nuclei and formed E rosettes with sheep RBCs. Virologic and biomolecular analysis revealed that all cases were infected with HTLV, and proviral DNA was integrated in host lymphocytes from 12 of the 14 cases examined. Furthermore, the lymphocyte populations, including abnormal T lymphocytes, were monoclonal with respect to the site of the provirus integration. Abnormal T lymphocytosis persisted from one to more than seven years in six cases, three of which developed ATL after a one- to five-year pre-ATL stage, whereas abnormal T lymphocytes spontaneously decreased in the other seven patients. However, HTLV-infected monoclonal lymphocytes were detected in four cases examined, even after most of the abnormal T lymphocytes had disappeared. Moreover, the same clonally provirus-integrated lymphocytes persisted in two of four cases not only during the course of abnormal lymphocytosis, but also in the subsequent almost-normal blood. These results indicate that the majority of the cases were in a pre-ATL state with a potential to develop ATL.

Adult↗
PubMed1985

Mother-to-child transmission of human T-cell leukemia virus type-I.

By screening sera obtained from 5015 pregnant women under the care of 9 gynecology/obstetrics departments of hospitals or clinics in Nagasaki City and its surrounding areas, 187 were found to be positive for antibody against adult T-cell leukemia-associated antigen (ATLA). The prevalence of seropositive pregnant women was consistent with that of blood donors in the age group of 16 to 29 years, taken as controls. Essentially all cord blood samples (113/115) of babies born from these seropositive mothers were positive for anti-ATLA of IgG class. These IgG antibodies in the babies diminished rapidly after delivery, and were detectable only in 3 cases at 2, 3, and 5 months of ages out of 38 babies up to 21 months. None of 115 cord bloods so far tested was positive either for anti-ATLA of IgM class or for ATLA-bearing lymphocytes after short-term cultures of the rosette-forming T-lymphocytes. Two of the babies born from 38 seropositive mothers were found seroconverted between the ages of 12 and 19 months. Three out of 20 elder siblings were found seropositive at ages of 3 to 6 years. The seropositive rate in these siblings was significantly higher than that of controls. Moreover, 12 out of 13 mothers traced back from seropositive students were found seropositive. These data indicate strongly that HTLV-I is transmitted from seropositive mothers to their children as a major pathway.

Age Factors↗
PubMed1985

Oral transmission of human T-cell leukemia virus type-I into a common marmoset (Callithrix jacchus) as an experimental model for milk-borne transmission.

To obtain experimental support for possible milk-borne infection of human T-cell leukemia virus type-I (HTLV-I), short-term-cultured viral antigen-positive lymphocytes obtained from peripheral blood of adult T-cell leukemia lymphoma complex (ATLL) patients were inoculated into the oral cavity of two adult common marmosets (Callithrix jacchus) in amounts comparable to those of HTLV-I-carrying cells fed to a baby in the milk of seropositive mothers. One of the animals seroconverted 2.5 months after the first inoculation. Cultures of peripheral blood mononuclear leukocytes of the marmoset revealed HTLV-I antigen expression in cells, indicating the establishment of oral infection of HTLV-I in an adult marmoset. The cell number deduced to be responsible for the infection was 5.6 X 10(7) cells (used in the first 2 inoculations). The results suggest that the concept of milk-borne infection of HTLV-I from a seropositive mother to her child is plausible.

Administration, Oral↗
PubMed1985

Oral infection of a common marmoset with human T-cell leukemia virus type-I (HTLV-I) by inoculating fresh human milk of HTLV-I carrier mothers.

To obtain definitive evidence that milk-borne infection plays a critical role in the endemy or mother-to-child transmission of human T-cell leukemia virus type-I (HTLV-I), we inoculated concentrated fresh human milk cells obtained from HTLV-I carrier mothers into the oral cavity of a common marmoset (Callithrix jacchus). Twenty-eight milk samples were collected (5-10 ml each) from 17 carrier mothers in the first week after delivery. Cells in the milk were centrifuged down and resuspended in 1/10 vol of the milk fluid. The concentrated cell suspensions were successively inoculated into the oral cavity of a common marmoset. The marmoset was found to be seroconverted by indirect immunofluorescence assay at 2.5 months after the first inoculation of the milk (3.5 X 10(8) cells in total), and was later confirmed to be infected with HTLV-I by the detection of viral antigen expression in short-term cultures of its peripheral blood T-lymphocytes. The results strongly support the working hypothesis that milk-borne infection plays a significant role in the mother-to-child transmission of HTLV-I.

Animals↗
PubMed1984

Detection of adult T-cell leukemia-associated antigen in T-cell malignancies in the Nagasaki district of Japan.

Adult T-cell leukemia-associated antigen (ATLA), a human retrovirus-associated antigen, and anti-ATLA antibodies were examined in 52 cases of T-cell malignancies in the Nagasaki district in southwestern Japan, which is known to be an ATL endemic area. These T-cell malignancies included 27 cases of ATL, 2 cases of T-cell chronic lymphocytic leukemia (T-CLL), 18 cases of T-cell lymphoma, and 5 cases of mycosis fungoides. Using the immunofluorescence method, ATLA-positive cells were detected in short-term mass culture of mononuclear cells from 22 of the 27 ATL patients, both T-CLL patients, 17 of 18 T-cell lymphoma patients, and 3 of the 5 mycosis fungoides patients. In an ATL patient in whom a high percentage of ATLA-positive cells were detected, many type C virus particles were observed in the extracellular space of the cultured mononuclear cells with an electron microscope. Sera from all 27 of the ATL patients, the 2 T-CLL patients, 15 of the 18 T-cell lymphoma patients, and 4 of the 5 mycosis fungoides patients were anti-ATLA antibody positive. These results indicate the possible participation of the retrovirus, ATL virus (ATLV), in these T-cell malignancies in ATL-endemic areas.

Adult↗
PubMed1984

Changes of adult T cell leukemia cell surface antigens at relapse or at exacerbation phase after chemotherapy defined by use of monoclonal antibodies.

Surface phenotypes of leukemic cells from six patients with adult T cell leukemia (ATL) were analyzed by the use of monoclonal antibodies, both at the time of initial diagnosis and at either relapse or exacerbation phase after chemotherapy. Changes of cell surface antigens were observed in four of the six cases. The majority of the leukemic cells of these patients were reactive with anti-Leu-1 and anti-Leu-3a, but unreactive with anti-Leu-2a and MAS 036c monoclonal antibodies at the time of initial diagnosis, indicating that ATL cells are of peripheral inducer/helper T cell origin. In three cases, the Leu-1 antigen disappeared at relapse or at exacerbation phase, and in one of these cases, a small percentage of ATL cells became reactive with MAS 036c, which identifies cortical thymocyte antigen. ATL cells of one other case did not have Leu-1 antigen from the start, but gained Leu-2a antigen at exacerbation phase and became double-labeled cells (Leu-2a+, 3a+), which is known to be a feature of thymocytes. Thus, it appeared that ATL cells sometimes change their surface phenotype to that of an earlier stage of T cell differentiation at relapse or at exacerbation phase. Chronic myelocytic leukemia (CML) cells also usually change to immature cells at blastic crisis involving morphological change. However, this morphological change was not so prominent in the ATL cases studied, except one, in which typical ATL cells with nuclear indentation changed to large immature cells with basophilic cytoplasm at relapse.

Adult↗
PubMed1983

Adult T-cell leukemia-lymphoma-related diseases in the Nagasaki District.

The clinical, hematological and pathological features of the adult T-cell leukemia (ATL)-related diseases and their cell membrane phenotypes in the Nagasaki district, one of the ATL-endemic areas, were delineated to compare them with those of adult T-cell leukemia-lymphoma (ATLL). In addition, the participation of ATL virus (ATLV) in the ATL-related diseases was investigated on the basis of a study of ATLV-associated antigen (ATLA) and anti-ATLA antibody. ATLA and/or anti-ATLA antibody could be detected in the ATL-related diseases, including persistent T-lymphocytosis with morphologically abnormal T-lymphocytes, T-cell chronic lymphocytic leukemia (T-CLL) of helper T-cells, T-cell malignant lymphoma of the skin, some seronegative helper T-cell malignant lymphomas and monomorphic T-cell leukemia with round nuclei. These results suggest that those cases in the Nagasaki district, though clinically different from each other, might be the same T-lymphoproliferative disease of possible viral etiology associated with ATLV. On the other hand, persistent T-lymphocytosis seems to be an infectious condition caused by ATLV and partly a preclinical stage of ATLL in view of the clinicohematological features.

Aged↗