Cancer immunoediting by the innate immune system in the absence of adaptive immunity
Cancer immunoediting is the process whereby immune cells protect against cancer formation by sculpting the immunogenicity of developing tumors. Although the full process depends on innate and adaptive immunity, it remains unclear whether innate immunity alone is capable of immunoediting. To determin...
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| Veröffentlicht in: | The Journal of experimental medicine 2012-09, Vol.209 (10), p.1869-1882 |
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| creator | O'Sullivan, Timothy Saddawi-Konefka, Robert Vermi, William Koebel, Catherine M Arthur, Cora White, J Michael Uppaluri, Ravi Andrews, Daniel M Ngiow, Shin Foong Teng, Michele W L Smyth, Mark J Schreiber, Robert D Bui, Jack D |
| description | Cancer immunoediting is the process whereby immune cells protect against cancer formation by sculpting the immunogenicity of developing tumors. Although the full process depends on innate and adaptive immunity, it remains unclear whether innate immunity alone is capable of immunoediting. To determine whether the innate immune system can edit tumor cells in the absence of adaptive immunity, we compared the incidence and immunogenicity of 3'methylcholanthrene-induced sarcomas in syngeneic wild-type, RAG2(-/-), and RAG2(-/-)x γc(-/-) mice. We found that innate immune cells could manifest cancer immunoediting activity in the absence of adaptive immunity. This activity required natural killer (NK) cells and interferon γ (IFN-γ), which mediated the induction of M1 macrophages. M1 macrophages could be elicited by administration of CD40 agonists, thereby restoring editing activity in RAG2(-/-)x γc(-/-) mice. Our results suggest that in the absence of adaptive immunity, NK cell production of IFN-γ induces M1 macrophages, which act as important effectors during cancer immunoediting. |
| doi_str_mv | 10.1084/jem.20112738 |
| format | Article |
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Although the full process depends on innate and adaptive immunity, it remains unclear whether innate immunity alone is capable of immunoediting. To determine whether the innate immune system can edit tumor cells in the absence of adaptive immunity, we compared the incidence and immunogenicity of 3'methylcholanthrene-induced sarcomas in syngeneic wild-type, RAG2(-/-), and RAG2(-/-)x γc(-/-) mice. We found that innate immune cells could manifest cancer immunoediting activity in the absence of adaptive immunity. This activity required natural killer (NK) cells and interferon γ (IFN-γ), which mediated the induction of M1 macrophages. M1 macrophages could be elicited by administration of CD40 agonists, thereby restoring editing activity in RAG2(-/-)x γc(-/-) mice. Our results suggest that in the absence of adaptive immunity, NK cell production of IFN-γ induces M1 macrophages, which act as important effectors during cancer immunoediting.</description><identifier>ISSN: 0022-1007</identifier><identifier>EISSN: 1540-9538</identifier><identifier>DOI: 10.1084/jem.20112738</identifier><identifier>PMID: 22927549</identifier><language>eng</language><publisher>United States: The Rockefeller University Press</publisher><subject>Adaptive Immunity ; Animals ; CD40 Antigens - agonists ; Cell Line, Tumor ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - immunology ; Genetic Predisposition to Disease ; Histocompatibility Antigens Class II - immunology ; Immunity, Innate ; Immunomodulation ; Interferon-gamma - biosynthesis ; Interleukin Receptor Common gamma Subunit - genetics ; Interleukin Receptor Common gamma Subunit - immunology ; Killer Cells, Natural - immunology ; Killer Cells, Natural - metabolism ; Macrophages - immunology ; Macrophages - metabolism ; Mice ; Mice, Knockout ; Neoplasms - genetics ; Neoplasms - immunology ; Neoplasms - mortality ; Phenotype ; Sarcoma - chemically induced ; Sarcoma - genetics ; Sarcoma - immunology ; Transplantation, Isogeneic</subject><ispartof>The Journal of experimental medicine, 2012-09, Vol.209 (10), p.1869-1882</ispartof><rights>2012 O’Sullivan et al. 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c483t-f718df2e92bf6ed87f312f93582b9fc20111a1bf0c85f7ec0289e9572745acd43</citedby><cites>FETCH-LOGICAL-c483t-f718df2e92bf6ed87f312f93582b9fc20111a1bf0c85f7ec0289e9572745acd43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22927549$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>O'Sullivan, Timothy</creatorcontrib><creatorcontrib>Saddawi-Konefka, Robert</creatorcontrib><creatorcontrib>Vermi, William</creatorcontrib><creatorcontrib>Koebel, Catherine M</creatorcontrib><creatorcontrib>Arthur, Cora</creatorcontrib><creatorcontrib>White, J Michael</creatorcontrib><creatorcontrib>Uppaluri, Ravi</creatorcontrib><creatorcontrib>Andrews, Daniel M</creatorcontrib><creatorcontrib>Ngiow, Shin Foong</creatorcontrib><creatorcontrib>Teng, Michele W L</creatorcontrib><creatorcontrib>Smyth, Mark J</creatorcontrib><creatorcontrib>Schreiber, Robert D</creatorcontrib><creatorcontrib>Bui, Jack D</creatorcontrib><title>Cancer immunoediting by the innate immune system in the absence of adaptive immunity</title><title>The Journal of experimental medicine</title><addtitle>J Exp Med</addtitle><description>Cancer immunoediting is the process whereby immune cells protect against cancer formation by sculpting the immunogenicity of developing tumors. Although the full process depends on innate and adaptive immunity, it remains unclear whether innate immunity alone is capable of immunoediting. To determine whether the innate immune system can edit tumor cells in the absence of adaptive immunity, we compared the incidence and immunogenicity of 3'methylcholanthrene-induced sarcomas in syngeneic wild-type, RAG2(-/-), and RAG2(-/-)x γc(-/-) mice. We found that innate immune cells could manifest cancer immunoediting activity in the absence of adaptive immunity. This activity required natural killer (NK) cells and interferon γ (IFN-γ), which mediated the induction of M1 macrophages. M1 macrophages could be elicited by administration of CD40 agonists, thereby restoring editing activity in RAG2(-/-)x γc(-/-) mice. Our results suggest that in the absence of adaptive immunity, NK cell production of IFN-γ induces M1 macrophages, which act as important effectors during cancer immunoediting.</description><subject>Adaptive Immunity</subject><subject>Animals</subject><subject>CD40 Antigens - agonists</subject><subject>Cell Line, Tumor</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - immunology</subject><subject>Genetic Predisposition to Disease</subject><subject>Histocompatibility Antigens Class II - immunology</subject><subject>Immunity, Innate</subject><subject>Immunomodulation</subject><subject>Interferon-gamma - biosynthesis</subject><subject>Interleukin Receptor Common gamma Subunit - genetics</subject><subject>Interleukin Receptor Common gamma Subunit - immunology</subject><subject>Killer Cells, Natural - immunology</subject><subject>Killer Cells, Natural - metabolism</subject><subject>Macrophages - immunology</subject><subject>Macrophages - metabolism</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Neoplasms - genetics</subject><subject>Neoplasms - immunology</subject><subject>Neoplasms - mortality</subject><subject>Phenotype</subject><subject>Sarcoma - chemically induced</subject><subject>Sarcoma - genetics</subject><subject>Sarcoma - immunology</subject><subject>Transplantation, Isogeneic</subject><issn>0022-1007</issn><issn>1540-9538</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkctLAzEQxoMotlZvnmWPHtyaZ5NcBCm-oOClnkM2O2lTurt1kxb637u1D_Q0MN9vvpnkQ-iW4CHBij8uoBpSTAiVTJ2hPhEc51owdY76GFOaE4xlD13FuMCYcC5Gl6hHqaZScN1H07GtHbRZqKp13UAZUqhnWbHN0hyyUNc2wV6DLG5jgqpr_mq2iNBNZo3PbGlXKWwOYEjba3Th7TLCzaEO0Nfry3T8nk8-3z7Gz5PcccVS7iVRpaegaeFHUCrpGaFeM6Foob3bPYpYUnjslPASHKZKgxaSSi6sKzkboKe972pdVFA6qFNrl2bVhsq2W9PYYP4rdZibWbMxjAspmegM7g8GbfO9hphMFaKD5dLW0KyjIUKQEadaqQ592KOubWJswZ_WEGx2QZguCHMMosPv_p52go8_z34ACxWFtA</recordid><startdate>20120924</startdate><enddate>20120924</enddate><creator>O'Sullivan, Timothy</creator><creator>Saddawi-Konefka, Robert</creator><creator>Vermi, William</creator><creator>Koebel, Catherine M</creator><creator>Arthur, Cora</creator><creator>White, J Michael</creator><creator>Uppaluri, Ravi</creator><creator>Andrews, Daniel M</creator><creator>Ngiow, Shin Foong</creator><creator>Teng, Michele W L</creator><creator>Smyth, Mark J</creator><creator>Schreiber, Robert D</creator><creator>Bui, Jack D</creator><general>The Rockefeller University Press</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>H94</scope><scope>5PM</scope></search><sort><creationdate>20120924</creationdate><title>Cancer immunoediting by the innate immune system in the absence of adaptive immunity</title><author>O'Sullivan, Timothy ; Saddawi-Konefka, Robert ; Vermi, William ; Koebel, Catherine M ; Arthur, Cora ; White, J Michael ; Uppaluri, Ravi ; Andrews, Daniel M ; Ngiow, Shin Foong ; Teng, Michele W L ; Smyth, Mark J ; Schreiber, Robert D ; Bui, Jack D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c483t-f718df2e92bf6ed87f312f93582b9fc20111a1bf0c85f7ec0289e9572745acd43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adaptive Immunity</topic><topic>Animals</topic><topic>CD40 Antigens - agonists</topic><topic>Cell Line, Tumor</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - immunology</topic><topic>Genetic Predisposition to Disease</topic><topic>Histocompatibility Antigens Class II - immunology</topic><topic>Immunity, Innate</topic><topic>Immunomodulation</topic><topic>Interferon-gamma - biosynthesis</topic><topic>Interleukin Receptor Common gamma Subunit - genetics</topic><topic>Interleukin Receptor Common gamma Subunit - immunology</topic><topic>Killer Cells, Natural - immunology</topic><topic>Killer Cells, Natural - metabolism</topic><topic>Macrophages - immunology</topic><topic>Macrophages - metabolism</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Neoplasms - genetics</topic><topic>Neoplasms - immunology</topic><topic>Neoplasms - mortality</topic><topic>Phenotype</topic><topic>Sarcoma - chemically induced</topic><topic>Sarcoma - genetics</topic><topic>Sarcoma - immunology</topic><topic>Transplantation, Isogeneic</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>O'Sullivan, Timothy</creatorcontrib><creatorcontrib>Saddawi-Konefka, Robert</creatorcontrib><creatorcontrib>Vermi, William</creatorcontrib><creatorcontrib>Koebel, Catherine M</creatorcontrib><creatorcontrib>Arthur, Cora</creatorcontrib><creatorcontrib>White, J Michael</creatorcontrib><creatorcontrib>Uppaluri, Ravi</creatorcontrib><creatorcontrib>Andrews, Daniel M</creatorcontrib><creatorcontrib>Ngiow, Shin Foong</creatorcontrib><creatorcontrib>Teng, Michele W L</creatorcontrib><creatorcontrib>Smyth, Mark J</creatorcontrib><creatorcontrib>Schreiber, Robert D</creatorcontrib><creatorcontrib>Bui, Jack D</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of experimental medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>O'Sullivan, Timothy</au><au>Saddawi-Konefka, Robert</au><au>Vermi, William</au><au>Koebel, Catherine M</au><au>Arthur, Cora</au><au>White, J Michael</au><au>Uppaluri, Ravi</au><au>Andrews, Daniel M</au><au>Ngiow, Shin Foong</au><au>Teng, Michele W L</au><au>Smyth, Mark J</au><au>Schreiber, Robert D</au><au>Bui, Jack D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cancer immunoediting by the innate immune system in the absence of adaptive immunity</atitle><jtitle>The Journal of experimental medicine</jtitle><addtitle>J Exp Med</addtitle><date>2012-09-24</date><risdate>2012</risdate><volume>209</volume><issue>10</issue><spage>1869</spage><epage>1882</epage><pages>1869-1882</pages><issn>0022-1007</issn><eissn>1540-9538</eissn><abstract>Cancer immunoediting is the process whereby immune cells protect against cancer formation by sculpting the immunogenicity of developing tumors. Although the full process depends on innate and adaptive immunity, it remains unclear whether innate immunity alone is capable of immunoediting. To determine whether the innate immune system can edit tumor cells in the absence of adaptive immunity, we compared the incidence and immunogenicity of 3'methylcholanthrene-induced sarcomas in syngeneic wild-type, RAG2(-/-), and RAG2(-/-)x γc(-/-) mice. We found that innate immune cells could manifest cancer immunoediting activity in the absence of adaptive immunity. This activity required natural killer (NK) cells and interferon γ (IFN-γ), which mediated the induction of M1 macrophages. M1 macrophages could be elicited by administration of CD40 agonists, thereby restoring editing activity in RAG2(-/-)x γc(-/-) mice. Our results suggest that in the absence of adaptive immunity, NK cell production of IFN-γ induces M1 macrophages, which act as important effectors during cancer immunoediting.</abstract><cop>United States</cop><pub>The Rockefeller University Press</pub><pmid>22927549</pmid><doi>10.1084/jem.20112738</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adaptive Immunity Animals CD40 Antigens - agonists Cell Line, Tumor DNA-Binding Proteins - genetics DNA-Binding Proteins - immunology Genetic Predisposition to Disease Histocompatibility Antigens Class II - immunology Immunity, Innate Immunomodulation Interferon-gamma - biosynthesis Interleukin Receptor Common gamma Subunit - genetics Interleukin Receptor Common gamma Subunit - immunology Killer Cells, Natural - immunology Killer Cells, Natural - metabolism Macrophages - immunology Macrophages - metabolism Mice Mice, Knockout Neoplasms - genetics Neoplasms - immunology Neoplasms - mortality Phenotype Sarcoma - chemically induced Sarcoma - genetics Sarcoma - immunology Transplantation, Isogeneic |
| title | Cancer immunoediting by the innate immune system in the absence of adaptive immunity |
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