Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The presence of alpha-2-macroglobulin (alpha-2-M) on the surface of peripheral blood lymphocytes from normal human subjects and from patients with chronic lymphatic leukaemia (CLL) and with ataxia-teleangectasia was studied by indirect immunofluorescence technique. Same experiments were done on purified subpopulations of normal blood peripheral lymphocytes (B and T). The percentage of alpha-2-M bearing lymphocytes is 17 +/- 6% as regard to normal subjects (Ig-bearing cells are 14%): in CLL the percentage of alpha-2-M bearing cells generally is significantly lower than that of Ig-bearing cells (IgM-IgD). On selected subpopulations, 90% of alpha-2-M bearing cells are present among non T-cells and only 5% among T-cells (probably due to not absolute purification). Blocking experiments using anti-Ig sera did not affect significantly the percentage of alpha-2-M bearing cells and using anti-alpha-2-M sera did not affect that of Ig-bearing cells. The percentage of E-rosette forming cells is not affected by pretreatment of peripheral lymphocytes with anti-Ig and/or anti-alpha-2-M sera. Hypothesis is set forth that alpha-2-M bearing cells could be a lymphocytes subpopulation made by a subgroup of B-cells and by K-cells, taking part in that immunoregulatory system in which collaborate many serum alpha-globulins and T-suppresor cells.
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PMID:[Presence of alpha-2-macroglobulin on the membrane of peripheral human blood lymphocytes : a new lymphocyte maker]. 6 74

The expression and function of neural cell adhesion molecule (NCAM, CD56, Leu19) on leukaemic blasts was investigated. The expression of NCAM was frequent (64%) in 14 studied cases of acute myeloid leukaemia (AML) but not in chronic lymphocytic leukaemia (CLL: 1/3 cases positive) or immunocytoma (IC: no positivity). No correlation with the expression of other AM (intercellular adhesion molecule-1 (ICAM-1), leucocyte function antigen-1 (LFA-1). VLA beta chain) or with AML type, according to FAB classification, was observed. Blocking of NCAM with anti-Leu 19 MoAb on AML targets resulted in a significant decrease of their susceptibility to LAK killing and in inhibition of conjugate formation. In the case of B prolymphocytic leukaemia (B-PLL) which did not express ICAM-1 or LFA-1 but was NCAM+, a complete resistance to LAK activity and lack of conjugate formation was observed. Blocking of NCAM on LAK effectors did not decrease their cytotoxic activity. Our results suggest that NCAM, in the presence of other AM, may have a supportive role in adhesion of leukaemic targets to LAK effectors.
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PMID:A supportive role of neural cell adhesion molecule (NCAM) in adhesion between leukaemic blasts and cytotoxic lymphocytes. 137

Pretreatment of acute myeloblastic leukemia cells with the hemopoietic growth factor interleukin 3 (IL3) increased their susceptibility to lymphokine activated killing (LAK) but did not affect their constitutive resistance to native natural killer activity. In addition, IL3 treatment did not alter the LAK cell-mediated killing of CD34+ hemopoietic progenitors present in normal bone marrow. Increased 3H-thymidine uptake was generally observed after IL3 treatment. However, failure to proliferate in response to IL3, observed in some cases, did not prevent changes in LAK susceptibility. Enhanced lysis of IL3-treated leukemic cells was accompanied by a moderate increase of the effector-target binding. Increased LAK susceptibility was already observed at 18 h, while optimal cytolysis and expression of the cell adhesion molecule (CAM) LFA-3 (CD58) by IL3-treated AML cells were concomitantly observed at later culture times. In contrast, the CAM ICAM-1 (CD54) was not modulated by IL3, nor were significant changes in the expression of either CAMs observed in normal hemopoietic cells. Blocking experiments with the anti-CD58 monoclonal antibody demonstrated a variable neutralizing effect on the IL3-induced increase of LAK activity, depending on the leukemia cell studied. The effect described here, together with the known role of IL3 in normal hemopoiesis makes it a factor of potential therapeutic value for the treatment of leukemic patients.
Leukemia 1992 Jun
PMID:Effect of human interleukin 3 on the susceptibility of fresh leukemia cells to interleukin-2-induced lymphokine activated killing activity. 137 79

Interleukin (IL) 1 is an important mediator of local and systemic disease. Blocking IL-1 using the IL-1 receptor antagonist has reduced the severity of disease in animal models of septic shock, diabetes, graft-vs-host disease, inflammatory bowel disease, and the spontaneous proliferation of leukemia cells. Blocking IL-1 and reduction in the synthesis of IL-1 are important strategies for reducing the progression of inflammatory disease and autoimmune diseases. Nature, however, maintains control over the synthesis of IL-1 by dissociating transcription for translation. In this paper, the basis for the dissociation of IL-1 beta synthesis of mRNA from synthesis of the IL-1 beta protein is reviewed.
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PMID:Dissociation of transcription from translation of human IL-1 beta: induction of steady state mRNA by adherence or recombinant C5a in the absence of translation. 153 18

We have examined subfractions of human thymocytes for the expression of novel differentiation antigens. Non-HLA alloantisera procured from multiparous women served as antibody probes. Thymocytes from five individuals were sequentially separated by discontinuous Percoll density gradient centrifugation and a peanut agglutinin (PNA) panning technique. Subfractions were selected and examined for their relative intensity of HLA class I and CD1 antigens as determined by cytofluorometric analysis. Two subfractions were characterized as follows: an immature population (Fr6 PNA-) expressed a high level of CD1 (OKT6 binding) antigen and a low level of class I HLA antigen; and a more mature fraction (Fr3 PNA-) expressed minimal amounts of CD1 antigen and relatively high levels of HLA class I molecules. Fr6 PNA+ and Fr3 PNA- thymocytes were tested for their reactivity with a panel of non-HLA alloantibodies as determined by cytofluorometric analysis. We observed that three alloantibodies demonstrated strong fluorescence staining with Fr6 PNA+ thymocytes only, whereas three other alloantibodies reacted with both the Fr6 PNA+ and the Fr3 PNA- subfractions. All six alloantibodies failed to react with peripheral T cells. However, the six antibodies did react with a panel of cultured T lymphoblastoid leukemic cells and fresh leukemic T cells. Blocking studies demonstrated that these alloantibodies do not bind beta 2-microglobulin-associated determinants. These results suggest that the alloantibodies detect thymocyte differentiation antigens (TDA) that are shared by or are cross-reactive with antigens expressed on certain leukemia T cells. The non-beta 2m-associated TDA antigens are not expressed on normal resting T cells.
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PMID:Serological identification of thymocyte differentiation antigens. 245 87

In vivo administrations of anti-Lyt-2.2 (CD8) mAb and anti-L3T4 (CD4) mAb selectively eliminated CD8+ cells and CD4+ cells, respectively. The relative potencies of CD8+ cells and CD4+ cells and their roles in primary tumor rejections were studied by investigating the effects of these mAbs on tumor growth. CD8+ cells were themselves fully capable of mediating rejection in 5 different tumor rejection systems: two radiation leukemia virus (RadLV)-induced leukemias, B6RV2 and BALBRVD, a radiation-induced leukemia BALBRL male 1, and a plasmacytoma BALBMOPC-70A in CB6F1 mice, and a Friend virus-induced leukemia B6FBL-3 in B6 mice. On the other hand, CD4+ cells were capable of resisting tumor growth of B6FBL-3, but not of the other four tumors. Furthermore, for efficient rejection of CB6F1UV female 1 sarcoma by CB6F1 mice, synergy of CD8+ and CD4+ cells was necessary. Blocking of UV female 1 rejection was abrogated by delayed administration of anti-L3T4 (CD4) mAb but not anti-Lyt-2.2 (CD8) mAb, indicating the involvement of CD4+ cells in only the initial phase of rejection.
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PMID:The roles of CD8+ and CD4+ cells in tumor rejection. 257 3

A mouse monoclonal IgG2a antibody, M195, with reactivity restricted to early myeloid cells, acute non-lymphoid leukemia cells (ANLL), and monocytic cells is described. The antibody was derived from a mouse immunized with live human leukemic myeloblasts. Specificity of binding of mAb M195 was determined by protein-A red blood cell rosetting assays, immunoabsorption, radioimmunoassays with iodine-125 labeled M195 IgG and F(Ab)'2, and complement cytotoxicity with live human cells and cell lines representing a broad range of lineages and tissues. Antigen expression was restricted to myeloid and monocytic leukemia cell lines and a fraction of mature adherent monocytes. Mature myeloid cells, T and B cells, erythrocytes, and platelets were negative. The antigen was not expressed on adult human tissues in immunoperoxidase and immunofluorescence assays. Blocking antigen was not found in the serum of patients with ANLL. Ten thousand sites per cell were expressed on myeloid or monocytic leukemia cell lines and 5000 sites per cell on mature monocytes. M195 IgG bound to its antigen target with an avidity of 3 x 10(9) liters/mol and induced rapid modulation of the antigen. M195 IgG was able to effectively kill cells with rabbit or guinea pig complement, but not human complement. The antibody did not mediate antibody dependent cellular cytotoxicity. The molecular nature of the target antigen remains unknown but it appears to be carried on the CD33 protein p67. Because of its restricted distribution on myelomonocytic cells, mAb M195 may be useful in studying myeloid differentiation, in the clinical diagnosis of ANLL, in purging of bone marrow of ANLL, and/or in monoclonal antibody therapy in vivo.
Leukemia 1989 May
PMID:Restricted expression of an early myeloid and monocytic cell surface antigen defined by monoclonal antibody M195. 271 49

Autologous lymphocyte populations from different phases of chronic granulocytic leukaemia (CGL), acute myeloid leukaemia (AML) and preleukaemic disorders were compared for cytotoxic activity. 51Cr-release tests showed that T lymphocytes from the quiescent phase of CGL and from the remission phase of AML exerted cytotoxic activity against autologous tumour cells. Such activity was also found in patients with potentially preleukaemic haematological disorders characterized by cytopenia, but not in polycythaemia vera patients. In the majority of cases cytotoxic activity of T lymphocytes could be blocked by native gp70 antigens of gibbon ape leukaemia virus (GaLV) and baboon endogenous virus (BaEV). Blocking effect of carbohydrate-free gp70 as well as p15(E) antigens could be observed less frequently. The role of cell-mediated immune response to oncovirus antigens in the course of myeloproliferative diseases is discussed.
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PMID:Cytotoxic activity of lymphocyte subpopulations against autologous tumour cells in patients with myeloid leukaemias and preleukaemic disorders. 326 Jul 9

After transplantation of B6RV2 leukemia, initial tumor growth was followed by tumor regression in B6 (CB6F1) female, but not male, mice. This indicated that H-Y antigen is involved in B6RV2 rejection by syngeneic female recipient mice. In the case of another leukemia, BALB.RL male 1, and Ir gene, probably identical to the Rgv-1 gene, is responsible for RL male 1 rejection. Thus, F1 hybrids of BALB/c with certain other strains of mice can reject RL male 1. Using these two different systems of tumor rejection, we investigated the effects of in vivo administration of Lyt and Thy-1 monoclonal antibodies (mAb). Results showed that Lyt-2 and -3 mAb blocked both B6RV2 rejection by B6 female mice and BALB.RL male 1 rejection by CB6F1 mice. The specificity of blocking was confirmed by use of Lyt-2 and -3 mAb to reciprocal alleles and mice from B6 Lyt-congeneic stocks. No blocking was observed with Lyt-1 and Thy-1 mAb. The Lyt phenotype of T cells in lymphoid tissues from mice treated with mAb was then studied. Blocking of the Lyt-2+3+ population was observed in the lymph node and spleen, but not in the thymus. These results indicate the involvement of Lyt-2+3+ cells (or Lyt-2,3 antigen) in tumor rejection. The precise mechanism of blocking is unknown, but it was observed after even a single injection of Lyt-2,3 mAb on day 9 after tumor transplantation, suggesting that effector cells were functionally blocked, rather than that the generation of these cells was inhibited.
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PMID:Effect of in vivo administration of Lyt antibodies. Lyt phenotype of T cells in lymphoid tissues and blocking of tumor rejection. 387 34

Fc receptors on the surface of milk leukocytes from normal glands, bronchial leukocytes, mastocytoma P-815 cells, and murine leukemia L1210 cells were blocked significantly (P less than 0.01) by cavian and bovine milk collected from inflamed glands (mastitic milk), their wheys, and in vitro-prepared immune complexes composed of the whey from normal milk and serum. Blocking of Fc receptors indicated the presence of immune complexes in the mastitic milk and was detected by inhibition of rosette formation with sensitized erythrocytes or attachment of the aggregated immunoglobulin G. The binding of immune complexes to these cells was also determined by staining with fluorescein isothiocyanate-labeled protein A. As the mastitis subsided, the blocking effect of the mastitic milk also declined markedly. There was no significant difference in blocking capacity between mastitic milk and its whey. The blocking capacity of normal cavian or bovine milk and their wheys was insignificant. Whey from mastitic milk also inhibited phagocytosis of opsonized staphylococci by alveolar macrophages. We suggest that the blocking of Fc receptors on phagocytic cells adversely affects phagocytosis.
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PMID:Effect of immune complexes from mastitic milk on blocking of Fc receptors and phagocytosis. 391 77


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