Immunomodulation of human leukocytes by staphylococcal enterotoxin A: augmentation of natural killer cells and induction of suppressor cells |
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| Authors: | C D Platsoucas E L Oleszak R A Good |
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| Affiliation: | 1. Department of Dermatology and Venerology, Peking University First Hospital, Beijing, China;2. Beijing Key Laboratory of Molecular Diagnosis on Dermatoses, Beijing, China;3. National Clinical Research Center for Skin and Immune Diseases, Beijing, China;4. Department of Dermatology, Shandong University Qilu Hospital, Jinan, Shandong, China;5. Laboratory of Basic Medical Science, Shandong University Qilu Hospital, Jinan, Shandong, China;1. Columbia University Vagelos College of Physicians and Surgeons, New York, New York, USA;2. Department of Dermatology, Columbia University Irving Medical Center, New York, New York, USA;1. LEO Foundation Skin Immunology Research Center, University of Copenhagen, Copenhagen, Denmark;2. Department of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark;3. Micreos Human Health B.V., Bilthoven, the Netherlands;4. Micreos GmbH, Wädenswil, Switzerland;5. Department of Dermatology, Bispebjerg and Frederiksberg Hospital, Copenhagen, Denmark;6. Department of Dermatology, Aarhus University Hospital, Aarhus, Denmark;7. Department of Pathology, NYU School of Medicine, New York, New York, USA |
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| Abstract: | Staphylococcal enterotoxin A (SEA), a protein isolated from culture supernatants of Staphylococcus aureus, is a potent T-cell mitogen and an inducer of interferon-gamma (IFN-gamma). We report here that SEA exhibits a number of significant in vitro immunomodulatory functions. In vitro treatment of human peripheral blood monocyte-depleted lymphocytes with SEA resulted in significant augmentation of their natural killer cytotoxicity against target cells from hemopoietic (K562, Daudi) or solid (melanoma, lung, colon) human tumor cell lines. SEA was found to be more effective than interferons-alpha (natural or Escherichia coli-derived) in augmenting natural killer (NK) cytotoxicity of peripheral blood lymphocytes. Studies on the kinetics of the augmentation revealed a significant increase of NK within 3 hr of in vitro treatment with SEA at 37 degrees C. A neutralizing monoclonal antibody specific for human IFN-gamma did not affect the augmentation of natural killer cytotoxicity by SEA, suggesting that SEA augmented natural killer cytotoxicity primarily by a mechanism not involving induction of interferon-gamma. Furthermore, in vitro treatment with SEA resulted in significant augmentation of antibody-dependent cell-mediated cytotoxicity and of natural killer-like cytotoxicity, generated in mixed lymphocyte culture, against the K562 targets. Induction of suppressor cells to proliferative responses of autologous or allogeneic mononuclear cells to phytohemagglutinin (PHA) or to allogeneic cells in mixed lymphocyte culture was observed after in vitro treatment of peripheral blood mononuclear leukocytes with SEA for 24 or 48 hr at 37 degrees C. In addition, the presence of SEA in mixed lymphocyte cultures (MLC) resulted in significant inhibition of the generation of specific T-cell-mediated cytotoxicity in MLC. These results suggest that SEA, which may be involved in S. aureus infections and in treatment with extracorporeal perfusion systems over S. aureus columns, can regulate a number of significant lymphoid functions. |
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