A blast from the past: clearance of apoptotic cells regulates immune responses
Key Points Apoptosis, a programmed and physiological form of cell death, is known to shape the immune system by regulating populations of effector lymphocytes. However, the binding and ingestion of dying cells by monocytes/macrophages and dendritic cells can also influence immune responses markedly...
Gespeichert in:
| Veröffentlicht in: | Nature reviews. Immunology 2002-12, Vol.2 (12), p.965-975 |
|---|---|
| Hauptverfasser: | , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 975 |
|---|---|
| container_issue | 12 |
| container_start_page | 965 |
| container_title | Nature reviews. Immunology |
| container_volume | 2 |
| creator | Savill, John Dransfield, Ian Gregory, Chris Haslett, Chris |
| description | Key Points
Apoptosis, a programmed and physiological form of cell death, is known to shape the immune system by regulating populations of effector lymphocytes. However, the binding and ingestion of dying cells by monocytes/macrophages and dendritic cells can also influence immune responses markedly by inducing or suppressing inflammation. Therefore, dead cells, which are a reflection of an organism's immediate past, can control its immunological future.
Dying cells are recognized by phagocytes as being non-self, altered-self or non-motile self, using innate-immune recognition, scavenger receptors or immunoglobulin-superfamily molecules, respectively.
Cell clearance by apoptosis has anti-inflammatory properties, by suppressing the release of pro-inflammatory cytokines by monocytes/macrophages and by the direct release of immunosuppressive cytokines, such as interleukin-10 and transforming growth factor-β1, by apoptotic cells.
Dendritic-cell maturation and presentation of antigen are suppressed by the uptake of apoptotic cells, which leads to the promotion of tolerance.
Defects in the clearance of apoptotic cells are associated with spontaneous/persistent tissue inflammation and autoimmunity to cell contents.
Strategies to promote the safe, anti-inflammatory and immunosuppressive clearance of dying cells are discussed.
There is a need to understand the mechanisms that, under certain circumstances, paradoxically allow apoptotic cells to stimulate the release of pro-inflammatory cytokines, such as tumour-necrosis factor, by macrophages and that allow dendritic cells to present antigen derived from apoptotic cells.
Apoptosis, which is a programmed and physiological form of cell death, is known to shape the immune system by regulating populations of effector lymphocytes. However, the binding and ingestion of dying cells by monocytes/macrophages and dendritic cells can also influence immune responses markedly by enhancing or suppressing inflammation. Therefore, dead cells, which are a reflection of an organism's immediate past, can control its immunological future. |
| doi_str_mv | 10.1038/nri957 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_72739067</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A188903971</galeid><sourcerecordid>A188903971</sourcerecordid><originalsourceid>FETCH-LOGICAL-c535t-197bb8bcc14ffe5329d5f2770d214073e89d07e474ba6c576a8658e795a1e6373</originalsourceid><addsrcrecordid>eNqFkl1rHSEQhqU0NB9tf0KRXiT04qS6rqv27hDaJhBa6Me1uO54zgZXt-pC--9rOIfmg0LwQp155mVeHYReU3JOCZPvQxoVF8_QEW1Fu6Kipc__nRk7RMc53xBCu5p5gQ5p03aUd-oIfVnj3ptcsEtxwmULeK63D9h6MMkECzg6bOY4l1hGiy14n3GCzeJNgYzHaVoC1ECeY8iQX6IDZ3yGV_v9BP389PHHxeXq-uvnq4v19cpyxsuKKtH3sreWts4BZ40auGuEIENDWyIYSDUQAbX93nSWi87IjksQihsKHRPsBJ3udOcUfy2Qi57GfNucCRCXrEUjmCLd0yCtwoy0qoJvH4E3cUmhmtBNQyinrZQVOt9BG-NBj8HFkoyta4BptDGAG2t8TaVUhClBa8G7BwWVKfC7bMySs776_u0he3qP3YLxZZujX8pYn_a_oE0x5wROz2mcTPqjKdG306B301DBN3tPSz_BcIftv78CZzsg11TYQLoz_UjqL6D7uTw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>220151488</pqid></control><display><type>article</type><title>A blast from the past: clearance of apoptotic cells regulates immune responses</title><source>MEDLINE</source><source>Nature Journals Online</source><source>SpringerLink Journals - AutoHoldings</source><creator>Savill, John ; Dransfield, Ian ; Gregory, Chris ; Haslett, Chris</creator><creatorcontrib>Savill, John ; Dransfield, Ian ; Gregory, Chris ; Haslett, Chris</creatorcontrib><description>Key Points
Apoptosis, a programmed and physiological form of cell death, is known to shape the immune system by regulating populations of effector lymphocytes. However, the binding and ingestion of dying cells by monocytes/macrophages and dendritic cells can also influence immune responses markedly by inducing or suppressing inflammation. Therefore, dead cells, which are a reflection of an organism's immediate past, can control its immunological future.
Dying cells are recognized by phagocytes as being non-self, altered-self or non-motile self, using innate-immune recognition, scavenger receptors or immunoglobulin-superfamily molecules, respectively.
Cell clearance by apoptosis has anti-inflammatory properties, by suppressing the release of pro-inflammatory cytokines by monocytes/macrophages and by the direct release of immunosuppressive cytokines, such as interleukin-10 and transforming growth factor-β1, by apoptotic cells.
Dendritic-cell maturation and presentation of antigen are suppressed by the uptake of apoptotic cells, which leads to the promotion of tolerance.
Defects in the clearance of apoptotic cells are associated with spontaneous/persistent tissue inflammation and autoimmunity to cell contents.
Strategies to promote the safe, anti-inflammatory and immunosuppressive clearance of dying cells are discussed.
There is a need to understand the mechanisms that, under certain circumstances, paradoxically allow apoptotic cells to stimulate the release of pro-inflammatory cytokines, such as tumour-necrosis factor, by macrophages and that allow dendritic cells to present antigen derived from apoptotic cells.
Apoptosis, which is a programmed and physiological form of cell death, is known to shape the immune system by regulating populations of effector lymphocytes. However, the binding and ingestion of dying cells by monocytes/macrophages and dendritic cells can also influence immune responses markedly by enhancing or suppressing inflammation. Therefore, dead cells, which are a reflection of an organism's immediate past, can control its immunological future.</description><identifier>ISSN: 1474-1733</identifier><identifier>EISSN: 1474-1741</identifier><identifier>DOI: 10.1038/nri957</identifier><identifier>PMID: 12461569</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Animals ; Antigens ; Apoptosis ; Apoptosis - immunology ; Autoimmunity - immunology ; Biomedical and Life Sciences ; Biomedicine ; Cell death ; Dendritic Cells - immunology ; Humans ; Immune system ; Immune System - immunology ; Immunology ; Inflammation ; Inflammation - immunology ; Ingestion ; Lymphocytes ; Lymphocytes - immunology ; Macrophages - immunology ; Microscopy ; Monocytes - immunology ; Morphology ; Phagocytosis ; Physiology ; Plasma ; review-article</subject><ispartof>Nature reviews. Immunology, 2002-12, Vol.2 (12), p.965-975</ispartof><rights>Springer Nature Limited 2002</rights><rights>COPYRIGHT 2002 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Dec 2002</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c535t-197bb8bcc14ffe5329d5f2770d214073e89d07e474ba6c576a8658e795a1e6373</citedby><cites>FETCH-LOGICAL-c535t-197bb8bcc14ffe5329d5f2770d214073e89d07e474ba6c576a8658e795a1e6373</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/nri957$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/nri957$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12461569$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Savill, John</creatorcontrib><creatorcontrib>Dransfield, Ian</creatorcontrib><creatorcontrib>Gregory, Chris</creatorcontrib><creatorcontrib>Haslett, Chris</creatorcontrib><title>A blast from the past: clearance of apoptotic cells regulates immune responses</title><title>Nature reviews. Immunology</title><addtitle>Nat Rev Immunol</addtitle><addtitle>Nat Rev Immunol</addtitle><description>Key Points
Apoptosis, a programmed and physiological form of cell death, is known to shape the immune system by regulating populations of effector lymphocytes. However, the binding and ingestion of dying cells by monocytes/macrophages and dendritic cells can also influence immune responses markedly by inducing or suppressing inflammation. Therefore, dead cells, which are a reflection of an organism's immediate past, can control its immunological future.
Dying cells are recognized by phagocytes as being non-self, altered-self or non-motile self, using innate-immune recognition, scavenger receptors or immunoglobulin-superfamily molecules, respectively.
Cell clearance by apoptosis has anti-inflammatory properties, by suppressing the release of pro-inflammatory cytokines by monocytes/macrophages and by the direct release of immunosuppressive cytokines, such as interleukin-10 and transforming growth factor-β1, by apoptotic cells.
Dendritic-cell maturation and presentation of antigen are suppressed by the uptake of apoptotic cells, which leads to the promotion of tolerance.
Defects in the clearance of apoptotic cells are associated with spontaneous/persistent tissue inflammation and autoimmunity to cell contents.
Strategies to promote the safe, anti-inflammatory and immunosuppressive clearance of dying cells are discussed.
There is a need to understand the mechanisms that, under certain circumstances, paradoxically allow apoptotic cells to stimulate the release of pro-inflammatory cytokines, such as tumour-necrosis factor, by macrophages and that allow dendritic cells to present antigen derived from apoptotic cells.
Apoptosis, which is a programmed and physiological form of cell death, is known to shape the immune system by regulating populations of effector lymphocytes. However, the binding and ingestion of dying cells by monocytes/macrophages and dendritic cells can also influence immune responses markedly by enhancing or suppressing inflammation. Therefore, dead cells, which are a reflection of an organism's immediate past, can control its immunological future.</description><subject>Animals</subject><subject>Antigens</subject><subject>Apoptosis</subject><subject>Apoptosis - immunology</subject><subject>Autoimmunity - immunology</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell death</subject><subject>Dendritic Cells - immunology</subject><subject>Humans</subject><subject>Immune system</subject><subject>Immune System - immunology</subject><subject>Immunology</subject><subject>Inflammation</subject><subject>Inflammation - immunology</subject><subject>Ingestion</subject><subject>Lymphocytes</subject><subject>Lymphocytes - immunology</subject><subject>Macrophages - immunology</subject><subject>Microscopy</subject><subject>Monocytes - immunology</subject><subject>Morphology</subject><subject>Phagocytosis</subject><subject>Physiology</subject><subject>Plasma</subject><subject>review-article</subject><issn>1474-1733</issn><issn>1474-1741</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkl1rHSEQhqU0NB9tf0KRXiT04qS6rqv27hDaJhBa6Me1uO54zgZXt-pC--9rOIfmg0LwQp155mVeHYReU3JOCZPvQxoVF8_QEW1Fu6Kipc__nRk7RMc53xBCu5p5gQ5p03aUd-oIfVnj3ptcsEtxwmULeK63D9h6MMkECzg6bOY4l1hGiy14n3GCzeJNgYzHaVoC1ECeY8iQX6IDZ3yGV_v9BP389PHHxeXq-uvnq4v19cpyxsuKKtH3sreWts4BZ40auGuEIENDWyIYSDUQAbX93nSWi87IjksQihsKHRPsBJ3udOcUfy2Qi57GfNucCRCXrEUjmCLd0yCtwoy0qoJvH4E3cUmhmtBNQyinrZQVOt9BG-NBj8HFkoyta4BptDGAG2t8TaVUhClBa8G7BwWVKfC7bMySs776_u0he3qP3YLxZZujX8pYn_a_oE0x5wROz2mcTPqjKdG306B301DBN3tPSz_BcIftv78CZzsg11TYQLoz_UjqL6D7uTw</recordid><startdate>20021201</startdate><enddate>20021201</enddate><creator>Savill, John</creator><creator>Dransfield, Ian</creator><creator>Gregory, Chris</creator><creator>Haslett, Chris</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</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>ISR</scope><scope>3V.</scope><scope>7QR</scope><scope>7RV</scope><scope>7T5</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope></search><sort><creationdate>20021201</creationdate><title>A blast from the past: clearance of apoptotic cells regulates immune responses</title><author>Savill, John ; Dransfield, Ian ; Gregory, Chris ; Haslett, Chris</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c535t-197bb8bcc14ffe5329d5f2770d214073e89d07e474ba6c576a8658e795a1e6373</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Animals</topic><topic>Antigens</topic><topic>Apoptosis</topic><topic>Apoptosis - immunology</topic><topic>Autoimmunity - immunology</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell death</topic><topic>Dendritic Cells - immunology</topic><topic>Humans</topic><topic>Immune system</topic><topic>Immune System - immunology</topic><topic>Immunology</topic><topic>Inflammation</topic><topic>Inflammation - immunology</topic><topic>Ingestion</topic><topic>Lymphocytes</topic><topic>Lymphocytes - immunology</topic><topic>Macrophages - immunology</topic><topic>Microscopy</topic><topic>Monocytes - immunology</topic><topic>Morphology</topic><topic>Phagocytosis</topic><topic>Physiology</topic><topic>Plasma</topic><topic>review-article</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Savill, John</creatorcontrib><creatorcontrib>Dransfield, Ian</creatorcontrib><creatorcontrib>Gregory, Chris</creatorcontrib><creatorcontrib>Haslett, Chris</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Chemoreception Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><jtitle>Nature reviews. Immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Savill, John</au><au>Dransfield, Ian</au><au>Gregory, Chris</au><au>Haslett, Chris</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A blast from the past: clearance of apoptotic cells regulates immune responses</atitle><jtitle>Nature reviews. Immunology</jtitle><stitle>Nat Rev Immunol</stitle><addtitle>Nat Rev Immunol</addtitle><date>2002-12-01</date><risdate>2002</risdate><volume>2</volume><issue>12</issue><spage>965</spage><epage>975</epage><pages>965-975</pages><issn>1474-1733</issn><eissn>1474-1741</eissn><abstract>Key Points
Apoptosis, a programmed and physiological form of cell death, is known to shape the immune system by regulating populations of effector lymphocytes. However, the binding and ingestion of dying cells by monocytes/macrophages and dendritic cells can also influence immune responses markedly by inducing or suppressing inflammation. Therefore, dead cells, which are a reflection of an organism's immediate past, can control its immunological future.
Dying cells are recognized by phagocytes as being non-self, altered-self or non-motile self, using innate-immune recognition, scavenger receptors or immunoglobulin-superfamily molecules, respectively.
Cell clearance by apoptosis has anti-inflammatory properties, by suppressing the release of pro-inflammatory cytokines by monocytes/macrophages and by the direct release of immunosuppressive cytokines, such as interleukin-10 and transforming growth factor-β1, by apoptotic cells.
Dendritic-cell maturation and presentation of antigen are suppressed by the uptake of apoptotic cells, which leads to the promotion of tolerance.
Defects in the clearance of apoptotic cells are associated with spontaneous/persistent tissue inflammation and autoimmunity to cell contents.
Strategies to promote the safe, anti-inflammatory and immunosuppressive clearance of dying cells are discussed.
There is a need to understand the mechanisms that, under certain circumstances, paradoxically allow apoptotic cells to stimulate the release of pro-inflammatory cytokines, such as tumour-necrosis factor, by macrophages and that allow dendritic cells to present antigen derived from apoptotic cells.
Apoptosis, which is a programmed and physiological form of cell death, is known to shape the immune system by regulating populations of effector lymphocytes. However, the binding and ingestion of dying cells by monocytes/macrophages and dendritic cells can also influence immune responses markedly by enhancing or suppressing inflammation. Therefore, dead cells, which are a reflection of an organism's immediate past, can control its immunological future.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>12461569</pmid><doi>10.1038/nri957</doi><tpages>11</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1474-1733 |
| ispartof | Nature reviews. Immunology, 2002-12, Vol.2 (12), p.965-975 |
| issn | 1474-1733 1474-1741 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_72739067 |
| source | MEDLINE; Nature Journals Online; SpringerLink Journals - AutoHoldings |
| subjects | Animals Antigens Apoptosis Apoptosis - immunology Autoimmunity - immunology Biomedical and Life Sciences Biomedicine Cell death Dendritic Cells - immunology Humans Immune system Immune System - immunology Immunology Inflammation Inflammation - immunology Ingestion Lymphocytes Lymphocytes - immunology Macrophages - immunology Microscopy Monocytes - immunology Morphology Phagocytosis Physiology Plasma review-article |
| title | A blast from the past: clearance of apoptotic cells regulates immune responses |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-08T14%3A56%3A24IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=A%20blast%20from%20the%20past:%20clearance%20of%20apoptotic%20cells%20regulates%20immune%20responses&rft.jtitle=Nature%20reviews.%20Immunology&rft.au=Savill,%20John&rft.date=2002-12-01&rft.volume=2&rft.issue=12&rft.spage=965&rft.epage=975&rft.pages=965-975&rft.issn=1474-1733&rft.eissn=1474-1741&rft_id=info:doi/10.1038/nri957&rft_dat=%3Cgale_proqu%3EA188903971%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=220151488&rft_id=info:pmid/12461569&rft_galeid=A188903971&rfr_iscdi=true |