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DIVERGENT ROLES FOR Fc RECEPTORS AND COMPLEMENT IN VIVO
Recent results obtained in mice deficient in either FcRs or complement have revealed distinct functions for these two classes of molecules. While each is capable of interacting with antibodies or immune complexes, the two systems mediate distinct biological effector responses. Complement-deficient m...
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| Published in: | Annual review of immunology 1998-01, Vol.16 (1), p.421-432 |
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| Format: | Article |
| Language: | English |
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| container_end_page | 432 |
| container_issue | 1 |
| container_start_page | 421 |
| container_title | Annual review of immunology |
| container_volume | 16 |
| creator | Ravetch, Jeffrey V Clynes, Raphael A |
| description | Recent results obtained in mice deficient in either FcRs or complement have
revealed distinct functions for these two classes of molecules. While each is
capable of interacting with antibodies or immune complexes, the two systems
mediate distinct biological effector responses. Complement-deficient mice are
unable to mediate innate immune responses to several bacterial pathogens and
bacterial toxins, yet respond normally to the presence of cytotoxic antibodies
and pathogenic immune complexes. In contrast, FcR-deficient mice display no
defects in innate immunity or susceptibility to a variety of pathogens, yet
they are unable to mediate inflammatory responses to cytotoxic IgG antibodies
or IgG immune complexes, despite the presence of a normal complement system.
These results lead to the surprising conclusion that these two systems have
evolved distinct functions in host immunity, with complement and its receptors
mediating the interaction of natural antibodies (IgM) with pathogens to effect
protection, while FcRs couple the interaction of IgG antibodies to effector
cells to trigger inflammatory sequelae. These results necessitate a fundamental
revision of the role of these antibody-binding systems in the immune
response. |
| doi_str_mv | 10.1146/annurev.immunol.16.1.421 |
| format | article |
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revealed distinct functions for these two classes of molecules. While each is
capable of interacting with antibodies or immune complexes, the two systems
mediate distinct biological effector responses. Complement-deficient mice are
unable to mediate innate immune responses to several bacterial pathogens and
bacterial toxins, yet respond normally to the presence of cytotoxic antibodies
and pathogenic immune complexes. In contrast, FcR-deficient mice display no
defects in innate immunity or susceptibility to a variety of pathogens, yet
they are unable to mediate inflammatory responses to cytotoxic IgG antibodies
or IgG immune complexes, despite the presence of a normal complement system.
These results lead to the surprising conclusion that these two systems have
evolved distinct functions in host immunity, with complement and its receptors
mediating the interaction of natural antibodies (IgM) with pathogens to effect
protection, while FcRs couple the interaction of IgG antibodies to effector
cells to trigger inflammatory sequelae. These results necessitate a fundamental
revision of the role of these antibody-binding systems in the immune
response.</description><identifier>ISSN: 0732-0582</identifier><identifier>EISSN: 1545-3278</identifier><identifier>DOI: 10.1146/annurev.immunol.16.1.421</identifier><identifier>PMID: 9597136</identifier><identifier>CODEN: ARIMDU</identifier><language>eng</language><publisher>Palo Alto, CA 94303-0139: Annual Reviews</publisher><subject>anaphylaxis ; Animals ; Complement System Proteins - physiology ; glomerulonephritis ; Humans ; immune complex ; inflammation ; innate immunity ; Mice ; Receptors, Fc - physiology</subject><ispartof>Annual review of immunology, 1998-01, Vol.16 (1), p.421-432</ispartof><rights>Copyright © 1998 by Annual Reviews. All rights reserved</rights><rights>Copyright Annual Reviews, Inc. 1998</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.annualreviews.org/content/journals/10.1146/annurev.immunol.16.1.421?crawler=true&mimetype=application/pdf$$EPDF$$P50$$Gannualreviews$$H</linktopdf><linktohtml>$$Uhttps://www.annualreviews.org/content/journals/10.1146/annurev.immunol.16.1.421$$EHTML$$P50$$Gannualreviews$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,78274,78379</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9597136$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ravetch, Jeffrey V</creatorcontrib><creatorcontrib>Clynes, Raphael A</creatorcontrib><title>DIVERGENT ROLES FOR Fc RECEPTORS AND COMPLEMENT IN VIVO</title><title>Annual review of immunology</title><addtitle>Annu Rev Immunol</addtitle><description>Recent results obtained in mice deficient in either FcRs or complement have
revealed distinct functions for these two classes of molecules. While each is
capable of interacting with antibodies or immune complexes, the two systems
mediate distinct biological effector responses. Complement-deficient mice are
unable to mediate innate immune responses to several bacterial pathogens and
bacterial toxins, yet respond normally to the presence of cytotoxic antibodies
and pathogenic immune complexes. In contrast, FcR-deficient mice display no
defects in innate immunity or susceptibility to a variety of pathogens, yet
they are unable to mediate inflammatory responses to cytotoxic IgG antibodies
or IgG immune complexes, despite the presence of a normal complement system.
These results lead to the surprising conclusion that these two systems have
evolved distinct functions in host immunity, with complement and its receptors
mediating the interaction of natural antibodies (IgM) with pathogens to effect
protection, while FcRs couple the interaction of IgG antibodies to effector
cells to trigger inflammatory sequelae. These results necessitate a fundamental
revision of the role of these antibody-binding systems in the immune
response.</description><subject>anaphylaxis</subject><subject>Animals</subject><subject>Complement System Proteins - physiology</subject><subject>glomerulonephritis</subject><subject>Humans</subject><subject>immune complex</subject><subject>inflammation</subject><subject>innate immunity</subject><subject>Mice</subject><subject>Receptors, Fc - physiology</subject><issn>0732-0582</issn><issn>1545-3278</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><recordid>eNqFkUtrwkAQgJfSYq3tTyiEHnpLurO72U0OPYhGK1gj0XpdNpsNKEm0efTx7xsx9FAowsAc5pthZj6ELMAOAONPqiia0nw42zxvin3mAHfAYQQuUB9c5tqUCO8S9bGgxMauR67RTVXtMMY-paKHer7rC6C8j8R4tgmiabBYW1E4D1bWJIysibaiYBQs12G0soaLsTUKX5fz4PVIzRbWZrYJb9FVqrLK3HV5gN4mwXr0Ys_D6Ww0nNuKClbbLiSCgDZcAyimKQbNGKV-mgjf10InPCYkNkIY7Qkds9TwNqhKXaI8DDEdoMfT3EO5f29MVct8W2mTZaow-6aSwvc85hN8FgROXRCUteDDH3C3b8qiPUISDJxhzN0Wuu-gJs5NIg_lNlflt-z-1tafT_WjCJW1Krbms_rFAMujJtlpkp2mdgkJstV0rv-_PnlIUll_1fQHzKOaLw</recordid><startdate>19980101</startdate><enddate>19980101</enddate><creator>Ravetch, Jeffrey V</creator><creator>Clynes, Raphael A</creator><general>Annual Reviews</general><general>Annual Reviews, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>19980101</creationdate><title>DIVERGENT ROLES FOR Fc RECEPTORS AND COMPLEMENT IN VIVO</title><author>Ravetch, Jeffrey V ; 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revealed distinct functions for these two classes of molecules. While each is
capable of interacting with antibodies or immune complexes, the two systems
mediate distinct biological effector responses. Complement-deficient mice are
unable to mediate innate immune responses to several bacterial pathogens and
bacterial toxins, yet respond normally to the presence of cytotoxic antibodies
and pathogenic immune complexes. In contrast, FcR-deficient mice display no
defects in innate immunity or susceptibility to a variety of pathogens, yet
they are unable to mediate inflammatory responses to cytotoxic IgG antibodies
or IgG immune complexes, despite the presence of a normal complement system.
These results lead to the surprising conclusion that these two systems have
evolved distinct functions in host immunity, with complement and its receptors
mediating the interaction of natural antibodies (IgM) with pathogens to effect
protection, while FcRs couple the interaction of IgG antibodies to effector
cells to trigger inflammatory sequelae. These results necessitate a fundamental
revision of the role of these antibody-binding systems in the immune
response.</abstract><cop>Palo Alto, CA 94303-0139</cop><cop>4139 El Camino Way, P.O. Box 10139</cop><cop>USA</cop><pub>Annual Reviews</pub><pmid>9597136</pmid><doi>10.1146/annurev.immunol.16.1.421</doi><tpages>12</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0732-0582 |
| ispartof | Annual review of immunology, 1998-01, Vol.16 (1), p.421-432 |
| issn | 0732-0582 1545-3278 |
| language | eng |
| recordid | cdi_pubmed_primary_9597136 |
| source | Electronic Back Volume Collection (EBVC) |
| subjects | anaphylaxis Animals Complement System Proteins - physiology glomerulonephritis Humans immune complex inflammation innate immunity Mice Receptors, Fc - physiology |
| title | DIVERGENT ROLES FOR Fc RECEPTORS AND COMPLEMENT IN VIVO |
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