Cytotoxicity of CD56bright NK Cells towards Autologous Activated CD4+ T Cells Is Mediated through NKG2D, LFA-1 and TRAIL and Dampened via CD94/NKG2A
In mouse models of chronic inflammatory diseases, Natural Killer (NK) cells can play an immunoregulatory role by eliminating chronically activated leukocytes. Indirect evidence suggests that NK cells may also be immunoregulatory in humans. Two subsets of human NK cells can be phenotypically distingu...
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| description | In mouse models of chronic inflammatory diseases, Natural Killer (NK) cells can play an immunoregulatory role by eliminating chronically activated leukocytes. Indirect evidence suggests that NK cells may also be immunoregulatory in humans. Two subsets of human NK cells can be phenotypically distinguished as CD16+CD56dim and CD16dim/−CD56bright. An expansion in the CD56bright NK cell subset has been associated with clinical responses to therapy in various autoimmune diseases, suggesting an immunoregulatory role for this subset in vivo. Here we compared the regulation of activated human CD4+ T cells by CD56dim and CD56bright autologous NK cells in vitro. Both subsets efficiently killed activated, but not resting, CD4+ T cells. The activating receptor NKG2D, as well as the integrin LFA-1 and the TRAIL pathway, played important roles in this process. Degranulation by NK cells towards activated CD4+ T cells was enhanced by IL-2, IL-15, IL-12+IL-18 and IFN-α. Interestingly, IL-7 and IL-21 stimulated degranulation by CD56bright NK cells but not by CD56dim NK cells. NK cell killing of activated CD4+ T cells was suppressed by HLA-E on CD4+ T cells, as blocking the interaction between HLA-E and the inhibitory CD94/NKG2A NK cell receptor enhanced NK cell degranulation. This study provides new insight into CD56dim and CD56bright NK cell-mediated elimination of activated autologous CD4+ T cells, which potentially may provide an opportunity for therapeutic treatment of chronic inflammation. |
| doi_str_mv | 10.1371/journal.pone.0031959 |
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Indirect evidence suggests that NK cells may also be immunoregulatory in humans. Two subsets of human NK cells can be phenotypically distinguished as CD16+CD56dim and CD16dim/−CD56bright. An expansion in the CD56bright NK cell subset has been associated with clinical responses to therapy in various autoimmune diseases, suggesting an immunoregulatory role for this subset in vivo. Here we compared the regulation of activated human CD4+ T cells by CD56dim and CD56bright autologous NK cells in vitro. Both subsets efficiently killed activated, but not resting, CD4+ T cells. The activating receptor NKG2D, as well as the integrin LFA-1 and the TRAIL pathway, played important roles in this process. Degranulation by NK cells towards activated CD4+ T cells was enhanced by IL-2, IL-15, IL-12+IL-18 and IFN-α. Interestingly, IL-7 and IL-21 stimulated degranulation by CD56bright NK cells but not by CD56dim NK cells. NK cell killing of activated CD4+ T cells was suppressed by HLA-E on CD4+ T cells, as blocking the interaction between HLA-E and the inhibitory CD94/NKG2A NK cell receptor enhanced NK cell degranulation. This study provides new insight into CD56dim and CD56bright NK cell-mediated elimination of activated autologous CD4+ T cells, which potentially may provide an opportunity for therapeutic treatment of chronic inflammation.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0031959</identifier><identifier>PMID: 22384114</identifier><language>eng</language><publisher>San Francisco: Public Library of Science</publisher><subject>Animal models ; Apoptosis ; Arthritis ; Autoimmune diseases ; Biocompatibility ; Biology ; CD16 antigen ; CD4 antigen ; Cytokines ; Cytotoxicity ; Degranulation ; Disease ; Histocompatibility antigen HLA ; Immunology ; Immunoregulation ; Inflammation ; Inflammatory diseases ; Interleukin 12 ; Interleukin 15 ; Interleukin 18 ; Interleukin 2 ; Interleukin 21 ; Interleukin 7 ; Leukocytes ; LFA-1 antigen ; Ligands ; Lung cancer ; Lymphatic system ; Lymphocyte receptors ; Lymphocytes ; Lymphocytes T ; Medical research ; Multiple sclerosis ; Natural killer cells ; NKG2 antigen ; Regulation ; Sarcoidosis ; T cell receptors ; Toxicity ; Trends ; α-Interferon</subject><ispartof>PloS one, 2012-02, Vol.7 (2), p.e31959</ispartof><rights>2012 Nielsen et al. 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Indirect evidence suggests that NK cells may also be immunoregulatory in humans. Two subsets of human NK cells can be phenotypically distinguished as CD16+CD56dim and CD16dim/−CD56bright. An expansion in the CD56bright NK cell subset has been associated with clinical responses to therapy in various autoimmune diseases, suggesting an immunoregulatory role for this subset in vivo. Here we compared the regulation of activated human CD4+ T cells by CD56dim and CD56bright autologous NK cells in vitro. Both subsets efficiently killed activated, but not resting, CD4+ T cells. The activating receptor NKG2D, as well as the integrin LFA-1 and the TRAIL pathway, played important roles in this process. Degranulation by NK cells towards activated CD4+ T cells was enhanced by IL-2, IL-15, IL-12+IL-18 and IFN-α. Interestingly, IL-7 and IL-21 stimulated degranulation by CD56bright NK cells but not by CD56dim NK cells. NK cell killing of activated CD4+ T cells was suppressed by HLA-E on CD4+ T cells, as blocking the interaction between HLA-E and the inhibitory CD94/NKG2A NK cell receptor enhanced NK cell degranulation. This study provides new insight into CD56dim and CD56bright NK cell-mediated elimination of activated autologous CD4+ T cells, which potentially may provide an opportunity for therapeutic treatment of chronic inflammation.</description><subject>Animal models</subject><subject>Apoptosis</subject><subject>Arthritis</subject><subject>Autoimmune diseases</subject><subject>Biocompatibility</subject><subject>Biology</subject><subject>CD16 antigen</subject><subject>CD4 antigen</subject><subject>Cytokines</subject><subject>Cytotoxicity</subject><subject>Degranulation</subject><subject>Disease</subject><subject>Histocompatibility antigen HLA</subject><subject>Immunology</subject><subject>Immunoregulation</subject><subject>Inflammation</subject><subject>Inflammatory diseases</subject><subject>Interleukin 12</subject><subject>Interleukin 15</subject><subject>Interleukin 18</subject><subject>Interleukin 2</subject><subject>Interleukin 21</subject><subject>Interleukin 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one</jtitle><date>2012-02-22</date><risdate>2012</risdate><volume>7</volume><issue>2</issue><spage>e31959</spage><pages>e31959-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>In mouse models of chronic inflammatory diseases, Natural Killer (NK) cells can play an immunoregulatory role by eliminating chronically activated leukocytes. Indirect evidence suggests that NK cells may also be immunoregulatory in humans. Two subsets of human NK cells can be phenotypically distinguished as CD16+CD56dim and CD16dim/−CD56bright. An expansion in the CD56bright NK cell subset has been associated with clinical responses to therapy in various autoimmune diseases, suggesting an immunoregulatory role for this subset in vivo. Here we compared the regulation of activated human CD4+ T cells by CD56dim and CD56bright autologous NK cells in vitro. Both subsets efficiently killed activated, but not resting, CD4+ T cells. The activating receptor NKG2D, as well as the integrin LFA-1 and the TRAIL pathway, played important roles in this process. Degranulation by NK cells towards activated CD4+ T cells was enhanced by IL-2, IL-15, IL-12+IL-18 and IFN-α. Interestingly, IL-7 and IL-21 stimulated degranulation by CD56bright NK cells but not by CD56dim NK cells. NK cell killing of activated CD4+ T cells was suppressed by HLA-E on CD4+ T cells, as blocking the interaction between HLA-E and the inhibitory CD94/NKG2A NK cell receptor enhanced NK cell degranulation. This study provides new insight into CD56dim and CD56bright NK cell-mediated elimination of activated autologous CD4+ T cells, which potentially may provide an opportunity for therapeutic treatment of chronic inflammation.</abstract><cop>San Francisco</cop><pub>Public Library of Science</pub><pmid>22384114</pmid><doi>10.1371/journal.pone.0031959</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Animal models Apoptosis Arthritis Autoimmune diseases Biocompatibility Biology CD16 antigen CD4 antigen Cytokines Cytotoxicity Degranulation Disease Histocompatibility antigen HLA Immunology Immunoregulation Inflammation Inflammatory diseases Interleukin 12 Interleukin 15 Interleukin 18 Interleukin 2 Interleukin 21 Interleukin 7 Leukocytes LFA-1 antigen Ligands Lung cancer Lymphatic system Lymphocyte receptors Lymphocytes Lymphocytes T Medical research Multiple sclerosis Natural killer cells NKG2 antigen Regulation Sarcoidosis T cell receptors Toxicity Trends α-Interferon |
| title | Cytotoxicity of CD56bright NK Cells towards Autologous Activated CD4+ T Cells Is Mediated through NKG2D, LFA-1 and TRAIL and Dampened via CD94/NKG2A |
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