Perpetual Secretory Dysfunction of Natural Killer-like Cells1.2

SUMMARY Sarcoidosis Is an Immunopathogenlc disorder of uncertain cause. Because the regula· tlon of monocyte mobilization and function may be critical to granuloma formation in this disease, wa evaluated production of the cell-dlrected Inhibitor of monocyte leukotaxls (CDI·MLx) by periph. eral blood and bronchoalveolar lavege mononuclear cells from these patients. Cells obtained from either source during clinically active disease spontaneously produced this leukotactlc regulator in "/tro In amounts comparable to those achieved with maximal mitogenic stimulation of normal cells. Plasma leukotactic Inhibitory activity and spontaneous Inhibitor production ware significantly associated. Plasma Inhibitory activity and CDI·MLx production ware normal In patients whose dis· ease was Inactive. Spontaneous production continued for at least 7 days /n "/tro and could not be attributed to alterations in the absolute numbers of specific mononuclear cell populations. Partl· tioning of peripheral blood mononuclear cells by a combination of E·rosettlng and Immunoadher· ence techniques indicated, howaver, that CDI·MLx was produced by a subpopulatlon of natural killer· like cells that formed E·rosettes and bore the OKMI and Leu 7 membrane antigens.

[1]  P. B. Campbell,et al.  Natural killer-like cells produce the cell-directed inhibitor of monocyte leukotaxis, CDI-MLx, in vitro. , 1986, Cellular immunology.

[2]  G. Pizzolo,et al.  Phenotypical and functional analysis of natural killer cells in sarcoidosis. , 1985, Clinical immunology and immunopathology.

[3]  M. Ferrarini,et al.  Production of B cell growth factor by a Leu-7+, OKM1+ non-T cell with the features of large granular lymphocytes (LGL). , 1985, Journal of immunology.

[4]  P. Allavena,et al.  Subsets of human large granular lymphocytes (LGL) exhibit accessory cell functions. , 1985, Journal of Immunology.

[5]  K. Rühle,et al.  Ia-like antigens on T-cells and their subpopulations in pulmonary sarcoidosis and in hypersensitivity pneumonitis. Analysis of bronchoalveolar and blood lymphocytes. , 1985, The American review of respiratory disease.

[6]  C. Grandori,et al.  Decline of natural cytotoxicity of human lymphocytes following infection with human T-cell leukemia/lymphoma virus (HTLV). , 1985, Leukemia research.

[7]  R. Crystal,et al.  Enhanced alveolar macrophage-mediated antigen-induced T-lymphocyte proliferation in sarcoidosis. , 1985, The Journal of clinical investigation.

[8]  J. Werkmeister,et al.  In vitro generation of human activated lymphocyte killer cells: separate precursors and modes of generation of NK-like cells and "anomalous" killer cells. , 1984, Journal of immunology.

[9]  Y. Kataria,et al.  In vitro production of inhibitors of monocyte locomotion by the granuloma of sarcoidosis. , 1984, The American review of respiratory disease.

[10]  M. Chilosi,et al.  Evidence of cells bearing interleukin-2 receptor at sites of disease activity in sarcoid patients. , 1984, Clinical and experimental immunology.

[11]  S. L. Yang,et al.  NK cell activity and skin test antigen stimulation of NK like CMC in vitro are decreased to different degrees in pregnancy and sarcoidosis. , 1984, Clinical and experimental immunology.

[12]  P. Allavena,et al.  Human large granular lymphocytes are potent producers of interleukin-1 , 1984, Nature.

[13]  G. Trinchieri,et al.  Human natural killer cells: biologic and pathologic aspects. , 1984, Laboratory investigation; a journal of technical methods and pathology.

[14]  G. Rice,et al.  Viruses disrupt functions of human lymphocytes. Effects of measles virus and influenza virus on lymphocyte-mediated killing and antibody production , 1984, The Journal of experimental medicine.

[15]  Hunninghake Gw Release of interleukin-1 by alveolar macrophages of patients with active pulmonary sarcoidosis. , 1984 .

[16]  J. Ceuppens,et al.  Alveolar T-cell subsets in pulmonary sarcoidosis. Correlation with disease activity and effect of steroid treatment. , 1984, The American review of respiratory disease.

[17]  N. Schaaf-Lafontaine,et al.  Suppression of CTL responses in vitro by large granular T cells. , 1984, Immunology letters.

[18]  M. Chilosi,et al.  Distribution of natural killer cells in sarcoidosis. , 1984, Journal of clinical & laboratory immunology.

[19]  G. Hunninghake,et al.  Role of interleukin-2 release by lung T-cells in active pulmonary sarcoidosis. , 2015, The American review of respiratory disease.

[20]  L. Abruzzo,et al.  Homeostasis of the antibody response: immunoregulation by NK cells. , 1983, Science.

[21]  J. Djeu,et al.  Capacity of human large granular lymphocytes (LGL) to produce multiple lymphokines: interleukin 2, interferon, and colony stimulating factor. , 1983, Journal of immunology.

[22]  G F Babcock,et al.  Subpopulations of human natural killer cells defined by expression of the Leu-7 (HNK-1) and Leu-11 (NK-15) antigens. , 1983, Journal of immunology.

[23]  T. Whiteside,et al.  Tissue distribution of human NK cells studied with anti-Leu-7 monoclonal antibody. , 1983, Journal of immunology.

[24]  B. Stadler,et al.  Interleukin 2 dependence of human natural killer (NK) cell activity. , 1983, Journal of immunology.

[25]  J. Thomas,et al.  A defect of in vitro monocyte leukotaxis induced by cutaneous allograft rejection. , 1982, Cellular immunology.

[26]  T. Kishimoto,et al.  Depressed functions of T cells and the presence of suppressor macrophages in patients with sarcoidosis. , 1982, Clinical immunology and immunopathology.

[27]  K. Hopper,et al.  Immunoregulation by macrophages: differential secretion of prostaglandin E and interleukin 1 during infection with Salmonella enteritidis. , 1982, Cellular immunology.

[28]  M. Ferrarini,et al.  Large granular lymphocytes in human peripheral blood: ultrastructural and cytochemical characterization of the granules. , 1982, Blood.

[29]  R. Crystal,et al.  Pulmonary sarcoidosis: a disorder mediated by excess helper T-lymphocyte activity at sites of disease activity. , 1981, The New England journal of medicine.

[30]  M. Mcnicol,et al.  T gamma cells in sarcoidosis: E rosetting monocytes suppress lymphocyte transformation. , 1981, Clinical and experimental immunology.

[31]  M. Hansson,et al.  Human fetal thymus and bone marrow contain target cells for natural killer cells , 1981, European journal of immunology.

[32]  S. Targan,et al.  Mode of action of interferon-mediated modulation of natural killer cytotoxic activity: recruitment of pre-NK cells and enhanced kinetics of lysis. , 1980, Journal of immunology.

[33]  V. Ferrans,et al.  Maintenance of granuloma formation in pulmonary sarcoidosis by T lymphocytes within the lung. , 1980, The New England journal of medicine.

[34]  R. Crystal,et al.  Localization of the immune response in sarcoidosis. , 2015, The American review of respiratory disease.

[35]  R. Messner,et al.  Suppressor cell function in sarcoidosis. , 1979, Annals of internal medicine.

[36]  Campbell Pb Defective monocyte leukotaxis in sarcoidosis: possible relationship to a plasma factor. , 1977 .

[37]  B. Czarnetzki,et al.  Ultrastructure of inclusions in peripheral blood mononuclear cells in sarcoidosis. , 1975, The American journal of pathology.