Roles of interferon and cellular adhesion molecules in bacterial activation of human natural killer cells
Interaction of lipopolysaccharide (LPS) from enteric and oral bacteria with natural killer (NK) cells enhanced cytotoxicity against NK-sensitive and NK-resistant targets. This activation occurred without expansion of the NK cell population or without changes in the leukocyte function-associated anti...
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| Vydané v: | Infection and immunity Ročník 57; číslo 6; s. 1702 |
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| Médium: | Journal Article |
| Jazyk: | English |
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United States
01.06.1989
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| ISSN: | 0019-9567 |
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| Abstract | Interaction of lipopolysaccharide (LPS) from enteric and oral bacteria with natural killer (NK) cells enhanced cytotoxicity against NK-sensitive and NK-resistant targets. This activation occurred without expansion of the NK cell population or without changes in the leukocyte function-associated antigen family of cellular adhesion molecule (CAM) expression on NK cells. Significant interferon (IFN) titers were measured in LPS-lymphocyte supernatants, and antibody to IFN-alpha blocked LPS activation. LPS-induced NK cytotoxicity was inhibited by antibodies to individual alpha chains of CAM and, more profoundly, by antibody to the beta chain of CAM. However, LPS, when preincubated with NK cells, did not compete with subsequent anti-CAM antibody binding as detected by flow cytometry. Anti-CAM antibodies had no effect on NK activation by IFN, but antibodies to either CD11a or CD11c abrogated IFN production induced by LPS. These findings suggest that LPS binds NK cells at non-CAM sites, resulting in the release of IFN. IFN then acts in an autocrine manner independent of CAM to enhance NK cytotoxicity. Interaction of anti-CAM antibodies with CAM may provide a negative signal in regulating LPS-induced IFN production. |
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| AbstractList | Interaction of lipopolysaccharide (LPS) from enteric and oral bacteria with natural killer (NK) cells enhanced cytotoxicity against NK-sensitive and NK-resistant targets. This activation occurred without expansion of the NK cell population or without changes in the leukocyte function-associated antigen family of cellular adhesion molecule (CAM) expression on NK cells. Significant interferon (IFN) titers were measured in LPS-lymphocyte supernatants, and antibody to IFN-alpha blocked LPS activation. LPS-induced NK cytotoxicity was inhibited by antibodies to individual alpha chains of CAM and, more profoundly, by antibody to the beta chain of CAM. However, LPS, when preincubated with NK cells, did not compete with subsequent anti-CAM antibody binding as detected by flow cytometry. Anti-CAM antibodies had no effect on NK activation by IFN, but antibodies to either CD11a or CD11c abrogated IFN production induced by LPS. These findings suggest that LPS binds NK cells at non-CAM sites, resulting in the release of IFN. IFN then acts in an autocrine manner independent of CAM to enhance NK cytotoxicity. Interaction of anti-CAM antibodies with CAM may provide a negative signal in regulating LPS-induced IFN production. Interaction of lipopolysaccharide (LPS) from enteric and oral bacteria with natural killer (NK) cells enhanced cytotoxicity against NK-sensitive and NK-resistant targets. This activation occurred without expansion of the NK cell population or without changes in the leukocyte function-associated antigen family of cellular adhesion molecule (CAM) expression on NK cells. Significant interferon (IFN) titers were measured in LPS-lymphocyte supernatants, and antibody to IFN-alpha blocked LPS activation. LPS-induced NK cytotoxicity was inhibited by antibodies to individual alpha chains of CAM and, more profoundly, by antibody to the beta chain of CAM. However, LPS, when preincubated with NK cells, did not compete with subsequent anti-CAM antibody binding as detected by flow cytometry. Anti-CAM antibodies had no effect on NK activation by IFN, but antibodies to either CD11a or CD11c abrogated IFN production induced by LPS. These findings suggest that LPS binds NK cells at non-CAM sites, resulting in the release of IFN. IFN then acts in an autocrine manner independent of CAM to enhance NK cytotoxicity. Interaction of anti-CAM antibodies with CAM may provide a negative signal in regulating LPS-induced IFN production.Interaction of lipopolysaccharide (LPS) from enteric and oral bacteria with natural killer (NK) cells enhanced cytotoxicity against NK-sensitive and NK-resistant targets. This activation occurred without expansion of the NK cell population or without changes in the leukocyte function-associated antigen family of cellular adhesion molecule (CAM) expression on NK cells. Significant interferon (IFN) titers were measured in LPS-lymphocyte supernatants, and antibody to IFN-alpha blocked LPS activation. LPS-induced NK cytotoxicity was inhibited by antibodies to individual alpha chains of CAM and, more profoundly, by antibody to the beta chain of CAM. However, LPS, when preincubated with NK cells, did not compete with subsequent anti-CAM antibody binding as detected by flow cytometry. Anti-CAM antibodies had no effect on NK activation by IFN, but antibodies to either CD11a or CD11c abrogated IFN production induced by LPS. These findings suggest that LPS binds NK cells at non-CAM sites, resulting in the release of IFN. IFN then acts in an autocrine manner independent of CAM to enhance NK cytotoxicity. Interaction of anti-CAM antibodies with CAM may provide a negative signal in regulating LPS-induced IFN production. |
| Author | Lindemann, R A |
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| References | 2895743 - Infect Immun. 1988 May;56(5):1301-8 3093576 - J Immunol. 1986 Oct 15;137(8):2428-33 3130415 - J Dent Res. 1988 May;67(5):846-50 6166701 - J Exp Med. 1981 Mar 1;153(3):569-82 4325022 - Appl Microbiol. 1971 Apr;21(4):723-5 3924996 - J Immunol. 1985 Aug;135(2):1020-5 13712490 - Exp Cell Res. 1961 Feb;23:14-20 3261303 - J Dent Res. 1988 Aug;67(8):1131-5 2408801 - Clin Exp Immunol. 1985 May;60(2):274-84 954005 - Cancer Res. 1976 Oct;36(10):3842-6 3918100 - J Immunol. 1985 Mar;134(3):1493-7 2453465 - Infect Immun. 1988 Jun;56(6):1436-41 7334070 - J Clin Immunol. 1981 Jan;1(1):51-63 3100481 - Hum Immunol. 1987 Jan;18(1):3-37 3537192 - J Exp Med. 1986 Dec 1;164(6):1876-88 6348161 - J Immunol Methods. 1983 Jul 29;61(3):293-300 |
| References_xml | – reference: 2895743 - Infect Immun. 1988 May;56(5):1301-8 – reference: 13712490 - Exp Cell Res. 1961 Feb;23:14-20 – reference: 6166701 - J Exp Med. 1981 Mar 1;153(3):569-82 – reference: 3537192 - J Exp Med. 1986 Dec 1;164(6):1876-88 – reference: 4325022 - Appl Microbiol. 1971 Apr;21(4):723-5 – reference: 954005 - Cancer Res. 1976 Oct;36(10):3842-6 – reference: 3261303 - J Dent Res. 1988 Aug;67(8):1131-5 – reference: 6348161 - J Immunol Methods. 1983 Jul 29;61(3):293-300 – reference: 2408801 - Clin Exp Immunol. 1985 May;60(2):274-84 – reference: 3918100 - J Immunol. 1985 Mar;134(3):1493-7 – reference: 3924996 - J Immunol. 1985 Aug;135(2):1020-5 – reference: 7334070 - J Clin Immunol. 1981 Jan;1(1):51-63 – reference: 3093576 - J Immunol. 1986 Oct 15;137(8):2428-33 – reference: 3100481 - Hum Immunol. 1987 Jan;18(1):3-37 – reference: 2453465 - Infect Immun. 1988 Jun;56(6):1436-41 – reference: 3130415 - J Dent Res. 1988 May;67(5):846-50 |
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| SubjectTerms | Antibodies, Monoclonal - physiology Antigens, Bacterial - immunology Antigens, Surface - analysis Antigens, Surface - immunology Binding Sites, Antibody Binding, Competitive Cell Adhesion Molecules Cytotoxicity, Immunologic Humans Immune Sera - pharmacology Interferon Inducers - immunology Interferons - biosynthesis Interferons - immunology Interferons - physiology Killer Cells, Natural - immunology Killer Cells, Natural - metabolism Killer Cells, Natural - microbiology Lipopolysaccharides - immunology Lymphocyte Activation Receptors, Immunologic - analysis |
| Title | Roles of interferon and cellular adhesion molecules in bacterial activation of human natural killer cells |
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