Prevention of T-cell lymphoma in AKR/J mice.
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T-Cell Lymphoma
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Peripheral T-cell lymphoma
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Tリンパ球の酵素組織化学的同定法とされるacid α-naphthyl acetate esterase(ANAE)染色法を用いて, 悪性リンパ腫のT, B cell typeの検索を行ない, 次の結果をえた。 1) ANAE染色は, 手技的にE-EAC-rosette法より優れた点が多く, 悪性リンパ腫のT, B cell typeの同定法としては適当である。 2) 悪性リンパ腫についての検索結果: (1)Non-Hodgkin’s lymphoma(14例)は, nodular patternは全例B cell type, diffuse patternの大部分の症例は組織型と関係なくT cell typeであつた。(2)Hodgkin’s lymphoma(1例)はT cell typeを示した。(3)いわゆるmalignant cutaneous lymphoma(12例)では, Sézary症候群, 菌状息肉症はすべてT cell type, 他のcutaneous lymphomaもほとんどがT cell typeで, B cell typeはわずか1例であつた。(4)T cell lymphomaの大多数で, 腫瘍細胞の表皮内浸潤がみられ, neoplasticなT cellは皮膚, とくに“表皮”に親和性を有する。また, T cell lymphomaは白血化して特異疹を伴う例が多く, 末血以外にリンパ節, 皮膚にANAE染色でT′ patternを示すneoplastic T cellが多数出現する。
T-Cell Lymphoma
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With the aim of identifying some of the stages in the development of pre-T cells (cells of the T cell lineage before they enter the thymus), we have produced a large number of hybridomas by the fusion of BALB/c bone marrow cells, bone marrow cells from BALB/c-nu/nu mice, BALB/c fetal liver cells and BALB/c fetal thymocytes with the AKR thymoma BW5147. The hybridomas were selected for the expression of the Thy-1.2 antigen of the normal cell donor and for their ability to produce interleukin 2 (IL 2) upon co-culture with irradiated normal spleen cells. A set of these hybridomas is described in this communication. The hybridomas were then used to immunize rats and to generate monoclonal antibody-producing B cell hybridomas. Most, if not all, of the immunizing hybridomas were derived from pre-T cells as evidenced by the fact that they produce IL 2, and express some of the T cell markers (the Thy-1.2, Ly-1, Ly-2 or L3T4 antigens). The monoclonal antibodies were tested on a panel of pre-T cell hybridomas and on normal cells obtained from spleen, lymph nodes, thymus and bone marrow. The testing was carried out by the microcytotoxicity assay and flow cytometric analysis. Three groups of antibodies could be distinguished. Some antibodies were broadly reactive, being positive with virtually all the clones in the pre-T cell panel and with a substantial fraction of normal lymphoid cells. The identity of the antigens detected by these antibodies remains unknown but they do not seem to correspond to any of the known cell surface markers. Other antibodies reacted only with some of the pre-T cell clones and did not react at all with normal lymphoid cells obtained from adult animals. Finally, other antibodies still reacted only with a minor subpopulation of thymocytes or of thymocytes and bone marrow cells, as well as some of the pre-T cell clones; they did not react with spleen and lymph node cells. These antibodies might be specific for cells in the prethymic phase of the T cell differentiation pathway. They should prove useful for the identification of pre-T cell markers and hence for the isolation of pre-T cells and their functional analysis.
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The functional ontogeny of the interacting T cell and B cell4 populations in the antibody response to sheep erythrocytes (SRBC) was investigated in CBA mice. It was found that T cell function, as determined by the ability of test cells to interact with adult bone marrow cells, was not detectable in fetal or neonate liver or lung. Moreover, even in the thymus this function remained less than 10% of adult values until birth. At birth T cell function increased exponentially, reaching adult levels within 48 hr. Neonatally thymectomized mice reconstituted with thymus cells of various ages confirmed these results. By day 4 after birth, T cell function could be detected in the spleen. B cell function, as determined by the ability of test cells to interact with adult thymus cells, was detected in the neonate spleen from day one. Therefore, both B cell and T cell function was present in the spleen from day 4 after birth. B cell function also was found in the fetal and neonate liver. B cell function of fetal liver was only 1/6 that of adult bone marrow on fetal day 16, quickly surpassed adult bone marrow activity near birth, and then equalled adult bone marrow activity until day 6 after birth. The ontogeny of B cell and T cell function in the antibody response to SRBC appears to take place at separate times in the mouse. B cell function develops first, most probably from the most primitive stem cell. T cell function develops later, after a structural thymus is present. Migration of T cell lymphocytes to other lymphoid tissue shortly after birth is consistent with the data presented.
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Peripheral T cell lymphoma not otherwise specified (PTCL-NOS) comprises heterogeneous lymphoid malignancies characterized by pleomorphic lymphocytes and variable inflammatory cell-rich tumor microenvironment. Genetic drivers in PTCL-NOS include genomic alterations affecting the VAV1 oncogene; however, their specific role and mechanisms in PTCL-NOS remain incompletely understood. Here we show that expression of Vav1-Myo1f, a recurrent PTCL-associated VAV1 fusion, induces oncogenic transformation of CD4
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The growth of B-cell lymphoma, LSCC-RP9, in culture was inhibited by spleen cells from bursa-immunized agammaglobulinemic (A-gamma) chickens. This inhibition was mediated by suppressor T-cells. The growth of transplantable LSCT-RP6 B-cell lymphoma was suppressed in A-gamma chickens, while that of the control SPCT-RP11 T-cell tumor was not affected. Furthermore, the incidence and growth of the LSCT-RP6 tumor in normal recipients were decreased when it was co-transplanted with spleen cells from bursa immunized A-gamma chickens. The results suggest that suppressor T-cells inhibit the growth of B-cell lymphoma.
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The immunohistochemical detection of CD1c antigen is described in mantle zone B-cells of the tonsil, lymph node, and spleen, and also in the marginal zone B-cells of the spleen. CD1c expression was observed in most cases of low-grade, but in only a single case of high-grade, B-cell non-Hodgkin's lymphoma. It was not detected in germinal centre cells, nor in Epstein-Barr virus-transformed or Burkitt's lymphoma B-cell lines. This distribution suggests that CD1c expression may occur preferentially in slowly proliferating B-cell populations and does not support previous suggestions that CD1c is a human equivalent of the mouse thymus leukaemia antigens.
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The stimulation of cells in gut associated lymphoid tissue (GALT) by intestinal antigens can result either in immunity or tolerance to that antigen. The factors that determine which effect predominates are not understood, but the answer seems to lie in a better understanding of the cellular interactions and regulatory mechanisms in GALT. Induction of an immune response in GALT involves the same macrophage-T cell, T cell-T cell, and T cell-B cell interactions that have been described in other lymphoid tissues. Regulatory T cells have now heen shown to play an important role in controlling the immune response to intestinal antigens. The presence of helper T cells specific for the IgA isotype in Peyer's patches may partly explain the old observation that the intestinal route is preferential for this antibody class. The stimulation of suppressor T cells in GALT is responsible for many instances in which tolerance rather than immunisation has followed antigen feeding. Although there is experimental evidence supporting the idea that mucosal IgA immunity and systemic IgG tolerance can occur concomitantly after antigen feeding. recent data obtained after the feeding of a variety of protein antigens indicate that this is not the usual result. More commonly either immunity or tolerance occurs concomitantly in both mucosal and systemic systems after antigen feeding, suggesting that the suppressor cells mediating oral tolerance also suppress mucosal IgA responses.
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