A review of human diseases caused or exacerbated by aberrant complement activation
Abstract Complement is the backbone of our innate immune system. It is of ancient evolutionary origin, being traced back to horseshoe crabs 350 million years ago. It consists today of more than 25 proteins which must work together like clockwork in order to distinguish friend from foe. Self attack b...
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| Veröffentlicht in: | Neurobiology of aging 2017-04, Vol.52, p.12-22 |
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| creator | McGeer, Patrick L Lee, Moonhee McGeer, Edith G |
| description | Abstract Complement is the backbone of our innate immune system. It is of ancient evolutionary origin, being traced back to horseshoe crabs 350 million years ago. It consists today of more than 25 proteins which must work together like clockwork in order to distinguish friend from foe. Self attack by the complement system can occur whenever it fails to do so. This failure has been reported to occur in an estimated 22 human diseases. A significant number of these are chronic degenerative neurological disorders. In some, there is overwhelming evidence that complement self attack causes the disease. In many others, it is considered only to contribute to the overall pathology. Finding effective therapeutic agents should be a high priority for medical research. To date, the monoclonal antibody eculizumab is the only approved agent. Molecules under development include other monoclonal antibodies directed at C5, C3, and properdin, various aptamers to C3, and small molecules that are orally available. |
| doi_str_mv | 10.1016/j.neurobiolaging.2016.12.017 |
| format | Article |
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It is of ancient evolutionary origin, being traced back to horseshoe crabs 350 million years ago. It consists today of more than 25 proteins which must work together like clockwork in order to distinguish friend from foe. Self attack by the complement system can occur whenever it fails to do so. This failure has been reported to occur in an estimated 22 human diseases. A significant number of these are chronic degenerative neurological disorders. In some, there is overwhelming evidence that complement self attack causes the disease. In many others, it is considered only to contribute to the overall pathology. Finding effective therapeutic agents should be a high priority for medical research. To date, the monoclonal antibody eculizumab is the only approved agent. 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All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c441t-b75923eda49dbf38895f14d4d4f6ccc9d76247cfc74e9aff09310129302e11593</citedby><cites>FETCH-LOGICAL-c441t-b75923eda49dbf38895f14d4d4f6ccc9d76247cfc74e9aff09310129302e11593</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.neurobiolaging.2016.12.017$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28104543$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>McGeer, Patrick L</creatorcontrib><creatorcontrib>Lee, Moonhee</creatorcontrib><creatorcontrib>McGeer, Edith G</creatorcontrib><title>A review of human diseases caused or exacerbated by aberrant complement activation</title><title>Neurobiology of aging</title><addtitle>Neurobiol Aging</addtitle><description>Abstract Complement is the backbone of our innate immune system. It is of ancient evolutionary origin, being traced back to horseshoe crabs 350 million years ago. It consists today of more than 25 proteins which must work together like clockwork in order to distinguish friend from foe. Self attack by the complement system can occur whenever it fails to do so. This failure has been reported to occur in an estimated 22 human diseases. A significant number of these are chronic degenerative neurological disorders. In some, there is overwhelming evidence that complement self attack causes the disease. In many others, it is considered only to contribute to the overall pathology. Finding effective therapeutic agents should be a high priority for medical research. To date, the monoclonal antibody eculizumab is the only approved agent. Molecules under development include other monoclonal antibodies directed at C5, C3, and properdin, various aptamers to C3, and small molecules that are orally available.</description><subject>Amyotrophic Lateral Sclerosis - genetics</subject><subject>Amyotrophic Lateral Sclerosis - immunology</subject><subject>Antibodies, Monoclonal - therapeutic use</subject><subject>Antibodies, Monoclonal, Humanized - therapeutic use</subject><subject>Arthritis, Rheumatoid - genetics</subject><subject>Arthritis, Rheumatoid - immunology</subject><subject>Chronic Disease</subject><subject>Complement</subject><subject>Complement Activation - immunology</subject><subject>Complement Pathway, Alternative - genetics</subject><subject>Complement Pathway, Classical - genetics</subject><subject>Complement receptors</subject><subject>Complement-mediated diseases</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Macular Degeneration - genetics</subject><subject>Macular Degeneration - immunology</subject><subject>Membrane attack complex</subject><subject>Molecular Targeted Therapy</subject><subject>Multiple Sclerosis - genetics</subject><subject>Multiple Sclerosis - immunology</subject><subject>Neurodegenerative Diseases - drug therapy</subject><subject>Neurodegenerative Diseases - genetics</subject><subject>Neurodegenerative Diseases - immunology</subject><subject>Neurology</subject><subject>Parkinson Disease - genetics</subject><subject>Parkinson Disease - immunology</subject><subject>Receptors, Complement</subject><issn>0197-4580</issn><issn>1558-1497</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkVFrFTEQhYMo9lr9C5IHH3zZNbPJbjYgQilWhYLQKvgWssmk5rq7uSa7rfffm8utBX2SPCQTzpnhfEPIK2A1MOjebOsZ1xSHEEdzE-abuim_NTQ1A_mIbKBt-wqEko_JhoGSlWh7dkKe5bxljEkhu6fkpOmBiVbwDbk6owlvA97R6On3dTIzdSGjyZipNWtGR2Oi-MtYTINZSjnsqRkwJTMv1MZpN-KE5WnsEm7NEuL8nDzxZsz44v4-JV8v3n85_1hdfv7w6fzssrJCwFINslUNR2eEcoPnfa9aD8KV4ztrrXKya4S03kqBynjPFC_5G8VZgwCt4qfk9bHvLsWfK-ZFTyFbHEczY1yzhr6Dkr0FKNK3R6lNMeeEXu9SmEzaa2D6QFVv9d9U9YGqhkYXqsX-8n7SOkzoHsx_MBbBxVGAJW-hmXS2AWeLLiS0i3Yx_O-kd_80smOYgzXjD9xj3sY1zYWpBp2LQV8fNnxYMHSccc6-8d_mzabU</recordid><startdate>20170401</startdate><enddate>20170401</enddate><creator>McGeer, Patrick L</creator><creator>Lee, Moonhee</creator><creator>McGeer, Edith G</creator><general>Elsevier Inc</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>7X8</scope></search><sort><creationdate>20170401</creationdate><title>A review of human diseases caused or exacerbated by aberrant complement activation</title><author>McGeer, Patrick L ; Lee, Moonhee ; McGeer, Edith G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c441t-b75923eda49dbf38895f14d4d4f6ccc9d76247cfc74e9aff09310129302e11593</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Amyotrophic Lateral Sclerosis - genetics</topic><topic>Amyotrophic Lateral Sclerosis - immunology</topic><topic>Antibodies, Monoclonal - therapeutic use</topic><topic>Antibodies, Monoclonal, Humanized - therapeutic use</topic><topic>Arthritis, Rheumatoid - genetics</topic><topic>Arthritis, Rheumatoid - immunology</topic><topic>Chronic Disease</topic><topic>Complement</topic><topic>Complement Activation - immunology</topic><topic>Complement Pathway, Alternative - genetics</topic><topic>Complement Pathway, Classical - genetics</topic><topic>Complement receptors</topic><topic>Complement-mediated diseases</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Macular Degeneration - genetics</topic><topic>Macular Degeneration - immunology</topic><topic>Membrane attack complex</topic><topic>Molecular Targeted Therapy</topic><topic>Multiple Sclerosis - genetics</topic><topic>Multiple Sclerosis - immunology</topic><topic>Neurodegenerative Diseases - drug therapy</topic><topic>Neurodegenerative Diseases - genetics</topic><topic>Neurodegenerative Diseases - immunology</topic><topic>Neurology</topic><topic>Parkinson Disease - genetics</topic><topic>Parkinson Disease - immunology</topic><topic>Receptors, Complement</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>McGeer, Patrick L</creatorcontrib><creatorcontrib>Lee, Moonhee</creatorcontrib><creatorcontrib>McGeer, Edith G</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Neurobiology of aging</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>McGeer, Patrick L</au><au>Lee, Moonhee</au><au>McGeer, Edith G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A review of human diseases caused or exacerbated by aberrant complement activation</atitle><jtitle>Neurobiology of aging</jtitle><addtitle>Neurobiol Aging</addtitle><date>2017-04-01</date><risdate>2017</risdate><volume>52</volume><spage>12</spage><epage>22</epage><pages>12-22</pages><issn>0197-4580</issn><eissn>1558-1497</eissn><abstract>Abstract Complement is the backbone of our innate immune system. It is of ancient evolutionary origin, being traced back to horseshoe crabs 350 million years ago. It consists today of more than 25 proteins which must work together like clockwork in order to distinguish friend from foe. Self attack by the complement system can occur whenever it fails to do so. This failure has been reported to occur in an estimated 22 human diseases. A significant number of these are chronic degenerative neurological disorders. In some, there is overwhelming evidence that complement self attack causes the disease. In many others, it is considered only to contribute to the overall pathology. Finding effective therapeutic agents should be a high priority for medical research. To date, the monoclonal antibody eculizumab is the only approved agent. 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| subjects | Amyotrophic Lateral Sclerosis - genetics Amyotrophic Lateral Sclerosis - immunology Antibodies, Monoclonal - therapeutic use Antibodies, Monoclonal, Humanized - therapeutic use Arthritis, Rheumatoid - genetics Arthritis, Rheumatoid - immunology Chronic Disease Complement Complement Activation - immunology Complement Pathway, Alternative - genetics Complement Pathway, Classical - genetics Complement receptors Complement-mediated diseases Humans Internal Medicine Macular Degeneration - genetics Macular Degeneration - immunology Membrane attack complex Molecular Targeted Therapy Multiple Sclerosis - genetics Multiple Sclerosis - immunology Neurodegenerative Diseases - drug therapy Neurodegenerative Diseases - genetics Neurodegenerative Diseases - immunology Neurology Parkinson Disease - genetics Parkinson Disease - immunology Receptors, Complement |
| title | A review of human diseases caused or exacerbated by aberrant complement activation |
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