Modulation of natural killer and antibody-dependent cellular cytotoxicity by interferon and interleukin-2 in chronic myeloid leukemia patients in remission. 1989

M Dabholkar, and R Tatake, and K Amin, and S Advani, and S Gangal
Immunology Division, Tata Memorial Hospital, Tata Memorial Centre, Bombay, India.

Our earlier studies demonstrated that about 55% of chronic myeloid leukemia (CML) patients in remission exhibited impaired natural killer (NK) cytotoxicity (low NK responders) while antibody-dependent cellular cytotoxicity (ADCC) of these patients, on chicken red blood cells as targets, was within normal range. In this paper, we have attempted to modulate the NK cytotoxicity of CML patients in remission with interferon (IFN) and interleukin-2 (IL-2) singly or together. ADCC using K562 target-directed monoclonal antibody (MAb) 4.6E10 was also modulated by treating the effectors with IFN or IL-2. Pretreatment of nonadherent mononuclear cells from peripheral blood (NAPBMNC) with IFN or IL-2 was found to result in 20 and 21% increase in target cell lysis in case of healthy donors, 79 and 98% increase in case of CML normal NK responders, and 164 and 159% increase in case of CML low NK responders. Combined use of IFN and IL-2 potentiated further the lymphocytotoxicity to 25% in healthy donors, 135% in normal NK responder CML patients and 283% in low NK responder CML patients. This treatment resulted in restoration of cytotoxicity of the latter group of patients to a normal level. The augmentation was seen in 80-100% CML patients. Although ADCC with chicken red blood cells as targets was within normal range, ADCC mediated with MAb to K562 cells was significantly lower in CML low NK responders (24.5%) than CML normal NK responders (42.4%) and healthy donors (65.9%).(ABSTRACT TRUNCATED AT 250 WORDS)

UI MeSH Term Description Entries
D007370 Interferon Type I Interferon secreted by leukocytes, fibroblasts, or lymphoblasts in response to viruses or interferon inducers other than mitogens, antigens, or allo-antigens. They include alpha- and beta-interferons (INTERFERON-ALPHA and INTERFERON-BETA). Interferons Type I,Type I Interferon,Type I Interferons,Interferon, Type I,Interferons, Type I
D007376 Interleukin-2 A soluble substance elaborated by antigen- or mitogen-stimulated T-LYMPHOCYTES which induces DNA synthesis in naive lymphocytes. IL-2,Lymphocyte Mitogenic Factor,T-Cell Growth Factor,TCGF,IL2,Interleukin II,Interleukine 2,RU 49637,RU-49637,Ro-23-6019,Ro-236019,T-Cell Stimulating Factor,Thymocyte Stimulating Factor,Interleukin 2,Mitogenic Factor, Lymphocyte,RU49637,Ro 23 6019,Ro 236019,Ro236019,T Cell Growth Factor,T Cell Stimulating Factor
D007694 Killer Cells, Natural Bone marrow-derived lymphocytes that possess cytotoxic properties, classically directed against transformed and virus-infected cells. Unlike T CELLS; and B CELLS; NK CELLS are not antigen specific. The cytotoxicity of natural killer cells is determined by the collective signaling of an array of inhibitory and stimulatory CELL SURFACE RECEPTORS. A subset of T-LYMPHOCYTES referred to as NATURAL KILLER T CELLS shares some of the properties of this cell type. NK Cells,Natural Killer Cells,Cell, NK,Cell, Natural Killer,Cells, NK,Cells, Natural Killer,Killer Cell, Natural,NK Cell,Natural Killer Cell
D011994 Recombinant Proteins Proteins prepared by recombinant DNA technology. Biosynthetic Protein,Biosynthetic Proteins,DNA Recombinant Proteins,Recombinant Protein,Proteins, Biosynthetic,Proteins, Recombinant DNA,DNA Proteins, Recombinant,Protein, Biosynthetic,Protein, Recombinant,Proteins, DNA Recombinant,Proteins, Recombinant,Recombinant DNA Proteins,Recombinant Proteins, DNA
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000911 Antibodies, Monoclonal Antibodies produced by a single clone of cells. Monoclonal Antibodies,Monoclonal Antibody,Antibody, Monoclonal
D000920 Antibody-Dependent Cell Cytotoxicity The phenomenon of antibody-mediated target cell destruction by non-sensitized effector cells. The identity of the target cell varies, but it must possess surface IMMUNOGLOBULIN G whose Fc portion is intact. The effector cell is a "killer" cell possessing Fc receptors. It may be a lymphocyte lacking conventional B- or T-cell markers, or a monocyte, macrophage, or polynuclear leukocyte, depending on the identity of the target cell. The reaction is complement-independent. ADCC,Cytotoxicity, Antibody-Dependent Cell,Cell Cytoxicity, Antibody-Dependent,Antibody Dependent Cell Cytotoxicity,Antibody-Dependent Cell Cytotoxicities,Antibody-Dependent Cell Cytoxicities,Antibody-Dependent Cell Cytoxicity,Cell Cytotoxicities, Antibody-Dependent,Cell Cytotoxicity, Antibody-Dependent,Cell Cytoxicities, Antibody-Dependent,Cell Cytoxicity, Antibody Dependent,Cytotoxicities, Antibody-Dependent Cell,Cytotoxicity, Antibody Dependent Cell,Cytoxicities, Antibody-Dependent Cell,Cytoxicity, Antibody-Dependent Cell
D015464 Leukemia, Myelogenous, Chronic, BCR-ABL Positive Clonal hematopoetic disorder caused by an acquired genetic defect in PLURIPOTENT STEM CELLS. It starts in MYELOID CELLS of the bone marrow, invades the blood and then other organs. The condition progresses from a stable, more indolent, chronic phase (LEUKEMIA, MYELOID, CHRONIC PHASE) lasting up to 7 years, to an advanced phase composed of an accelerated phase (LEUKEMIA, MYELOID, ACCELERATED PHASE) and BLAST CRISIS. Granulocytic Leukemia, Chronic,Leukemia, Granulocytic, Chronic,Leukemia, Myelocytic, Chronic,Leukemia, Myelogenous, Chronic,Leukemia, Myeloid, Chronic,Myelocytic Leukemia, Chronic,Myelogenous Leukemia, Chronic,Myeloid Leukemia, Chronic,Leukemia, Chronic Myelogenous,Leukemia, Chronic Myeloid,Leukemia, Myelogenous, Ph1 Positive,Leukemia, Myelogenous, Ph1-Positive,Leukemia, Myeloid, Ph1 Positive,Leukemia, Myeloid, Ph1-Positive,Leukemia, Myeloid, Philadelphia Positive,Leukemia, Myeloid, Philadelphia-Positive,Myelogenous Leukemia, Ph1-Positive,Myeloid Leukemia, Ph1-Positive,Myeloid Leukemia, Philadelphia-Positive,Chronic Granulocytic Leukemia,Chronic Granulocytic Leukemias,Chronic Myelocytic Leukemia,Chronic Myelocytic Leukemias,Chronic Myelogenous Leukemia,Chronic Myelogenous Leukemias,Chronic Myeloid Leukemia,Chronic Myeloid Leukemias,Granulocytic Leukemias, Chronic,Leukemia, Chronic Granulocytic,Leukemia, Chronic Myelocytic,Leukemia, Ph1-Positive Myelogenous,Leukemia, Ph1-Positive Myeloid,Leukemia, Philadelphia-Positive Myeloid,Leukemias, Chronic Granulocytic,Leukemias, Chronic Myelocytic,Leukemias, Chronic Myelogenous,Leukemias, Chronic Myeloid,Leukemias, Ph1-Positive Myelogenous,Leukemias, Ph1-Positive Myeloid,Leukemias, Philadelphia-Positive Myeloid,Myelocytic Leukemias, Chronic,Myelogenous Leukemia, Ph1 Positive,Myelogenous Leukemias, Chronic,Myelogenous Leukemias, Ph1-Positive,Myeloid Leukemia, Ph1 Positive,Myeloid Leukemia, Philadelphia Positive,Myeloid Leukemias, Chronic,Myeloid Leukemias, Ph1-Positive,Myeloid Leukemias, Philadelphia-Positive,Ph1-Positive Myelogenous Leukemia,Ph1-Positive Myelogenous Leukemias,Ph1-Positive Myeloid Leukemia,Ph1-Positive Myeloid Leukemias,Philadelphia-Positive Myeloid Leukemia,Philadelphia-Positive Myeloid Leukemias

Related Publications

M Dabholkar, and R Tatake, and K Amin, and S Advani, and S Gangal
December 1982, Agents and actions,
M Dabholkar, and R Tatake, and K Amin, and S Advani, and S Gangal
January 1986, Cancer immunology, immunotherapy : CII,
M Dabholkar, and R Tatake, and K Amin, and S Advani, and S Gangal
July 1989, Nihon Ketsueki Gakkai zasshi : journal of Japan Haematological Society,
M Dabholkar, and R Tatake, and K Amin, and S Advani, and S Gangal
May 1998, Cellular immunology,
M Dabholkar, and R Tatake, and K Amin, and S Advani, and S Gangal
June 1990, International journal of leprosy and other mycobacterial diseases : official organ of the International Leprosy Association,
M Dabholkar, and R Tatake, and K Amin, and S Advani, and S Gangal
October 1984, Journal of clinical & laboratory immunology,
M Dabholkar, and R Tatake, and K Amin, and S Advani, and S Gangal
June 1993, Gut,
M Dabholkar, and R Tatake, and K Amin, and S Advani, and S Gangal
January 1982, Cancer immunology, immunotherapy : CII,
Copied contents to your clipboard!