{"id":{"repo_id":"ohiolink","oai_identifier":"oai:etd.ohiolink.edu:case1346268879"},"canonical_url":"https://search.dev.ndltd.org/etd/ohiolink/oai:etd.ohiolink.edu:case1346268879","repository":{"repo_id":"ohiolink","name":"OhioLINK","base_url":"https://etd.ohiolink.edu/acprod/odb_etd/ws/oai/oai"},"display":{"title":"Bidirectional Natural Killer Cell and Dendritic Cell Interactions in HIV-1 Pathogenesis","abstract":"Natural killer (NK) and dendritic cell (DC) interactions are pivotal for the development of immune responses, which lead to bidirectional NK:DC activation. In HIV-1 infection, both NK cell and DC function are impaired, resulting in dysfunctional NK:DC crosstalk. We demonstrate that NK:DC interactions result in the induction of CD4 expression on NK cells, thereby increasing NK cell susceptibility to HIV-1 infection. Furthermore, we show that NK:DC interactions influence NK cell degranulation.CD4+ NK cells mediate DC maturation via cell-cell contact interactions and soluble factors. We find that CD4+ NK cells are more efficient at inducing DC maturation than CD4- NK cells, suggesting that CD4 is an activation marker on NK cells. CD4+ NK cells also influence DC function as they decrease DC macropinocytotic capacity, which is characteristic of DC maturation. NK:DC interactions affect HIV-1 infection, as NK-mature DCs effectively deliver HIV-1 to T cells via trans-infection. DC-mediated induction of CD4 expression on NK cells renders NK cells susceptible to HIV-1 infection. Furthermore, DCs can transfer infectious viruses and enhance HIV-1 infection of CD4+ NK cells.Our findings provide new insights regarding NK:DC interactions, defining a mechanism by which cellular interactions in the absence of pathogens promote DC-mediated amplification of HIV-1 infection. These findings provide a new mechanism by which CD4 expression can be induced in vivo, resulting in HIV-1 infection of NK cells.","abstract_html":"Natural killer (NK) and dendritic cell (DC) interactions are pivotal for the development of immune responses, which lead to bidirectional NK:DC activation. In HIV-1 infection, both NK cell and DC function are impaired, resulting in dysfunctional NK:DC crosstalk. We demonstrate that NK:DC interactions result in the induction of CD4 expression on NK cells, thereby increasing NK cell susceptibility to HIV-1 infection. Furthermore, we show that NK:DC interactions influence NK cell degranulation.CD4+ NK cells mediate DC maturation via cell-cell contact interactions and soluble factors. We find that CD4+ NK cells are more efficient at inducing DC maturation than CD4- NK cells, suggesting that CD4 is an activation marker on NK cells. CD4+ NK cells also influence DC function as they decrease DC macropinocytotic capacity, which is characteristic of DC maturation. NK:DC interactions affect HIV-1 infection, as NK-mature DCs effectively deliver HIV-1 to T cells via trans-infection. DC-mediated induction of CD4 expression on NK cells renders NK cells susceptible to HIV-1 infection. Furthermore, DCs can transfer infectious viruses and enhance HIV-1 infection of CD4+ NK cells.Our findings provide new insights regarding NK:DC interactions, defining a mechanism by which cellular interactions in the absence of pathogens promote DC-mediated amplification of HIV-1 infection. These findings provide a new mechanism by which CD4 expression can be induced in vivo, resulting in HIV-1 infection of NK cells.","abstract_has_math":false,"creators":["Valentin-Torres, Alice M."],"institution":"Case Western Reserve University School of Graduate Studies","degree_name":"Doctor of Philosophy","degree_level":"doctoral","degree_discipline":"Molecular Biology and Microbiology","degree_department":null,"school":null,"contributors":["Bernstein, Helene","McDonald, David"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2013,"date_issued":"2013-03-12","date_published":"2013-03-12","updated_at":"2026-07-24T03:35:52Z","subjects":["Immunology","Molecular Biology","Virology","HIV","NK cell","Dendritic Cells","bidirectional interactionsi"],"languages":["English"],"rights":["unrestricted","This thesis or dissertation is protected by copyright: all rights reserved. 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We find that CD4+ NK cells are more efficient at inducing DC maturation than CD4- NK cells, suggesting that CD4 is an activation marker on NK cells. CD4+ NK cells also influence DC function as they decrease DC macropinocytotic capacity, which is characteristic of DC maturation. NK:DC interactions affect HIV-1 infection, as NK-mature DCs effectively deliver HIV-1 to T cells via trans-infection. DC-mediated induction of CD4 expression on NK cells renders NK cells susceptible to HIV-1 infection. Furthermore, DCs can transfer infectious viruses and enhance HIV-1 infection of CD4+ NK cells.Our findings provide new insights regarding NK:DC interactions, defining a mechanism by which cellular interactions in the absence of pathogens promote DC-mediated amplification of HIV-1 infection. These findings provide a new mechanism by which CD4 expression can be induced in vivo, resulting in HIV-1 infection of NK cells."]},{"key":"dc:format","label":"Dc Format","values":["application/pdf","p.171","3.28 MB"]},{"key":"dc:title","label":"Title","values":["Bidirectional Natural Killer Cell and Dendritic Cell Interactions in HIV-1 Pathogenesis"]}]}],"canonical_facts":{"dc:contributor":["Bernstein, Helene","McDonald, David"],"dc:creator":["Valentin-Torres, Alice M."],"dc:date":["2013-03-12"],"dc:description":["Natural killer (NK) and dendritic cell (DC) interactions are pivotal for the development of immune responses, which lead to bidirectional NK:DC activation. In HIV-1 infection, both NK cell and DC function are impaired, resulting in dysfunctional NK:DC crosstalk. We demonstrate that NK:DC interactions result in the induction of CD4 expression on NK cells, thereby increasing NK cell susceptibility to HIV-1 infection. Furthermore, we show that NK:DC interactions influence NK cell degranulation.CD4+ NK cells mediate DC maturation via cell-cell contact interactions and soluble factors. We find that CD4+ NK cells are more efficient at inducing DC maturation than CD4- NK cells, suggesting that CD4 is an activation marker on NK cells. CD4+ NK cells also influence DC function as they decrease DC macropinocytotic capacity, which is characteristic of DC maturation. NK:DC interactions affect HIV-1 infection, as NK-mature DCs effectively deliver HIV-1 to T cells via trans-infection. DC-mediated induction of CD4 expression on NK cells renders NK cells susceptible to HIV-1 infection. Furthermore, DCs can transfer infectious viruses and enhance HIV-1 infection of CD4+ NK cells.Our findings provide new insights regarding NK:DC interactions, defining a mechanism by which cellular interactions in the absence of pathogens promote DC-mediated amplification of HIV-1 infection. These findings provide a new mechanism by which CD4 expression can be induced in vivo, resulting in HIV-1 infection of NK cells."],"dc:format":["application/pdf","p.171","3.28 MB"],"dc:identifier":["http://rave.ohiolink.edu/etdc/view?acc_num=case1346268879"],"dc:language":["English"],"dc:publisher":["Case Western Reserve University School of Graduate Studies / OhioLINK"],"dc:rights":["unrestricted","This thesis or dissertation is protected by copyright: all rights reserved. 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