Autoimmunity is a type I interferon-deficiency syndrome corrected by ingested type I IFN via the GALT system
Type I interferons (IFN-alpha/beta), products of the innate immune system, can modulate immune function whereas proinflammatory IFN-gamma (type II IFN), a product of the acquired immune system upregulates inflammation and enhances cell mediated immunity. We have proposed a unifying hypothesis of the...
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Veröffentlicht in: | Journal of interferon & cytokine research 1999-08, Vol.19 (8), p.841-852 |
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description | Type I interferons (IFN-alpha/beta), products of the innate immune system, can modulate immune function whereas proinflammatory IFN-gamma (type II IFN), a product of the acquired immune system upregulates inflammation and enhances cell mediated immunity. We have proposed a unifying hypothesis of the origin of autoimmunity as a type I IFN immunodeficiency syndrome involving inadequate regulation of the acquired immune system product IFN-gamma by the IFN-alpha/beta innate immune system. The common theme of ingested type I IFNs in autoimmunity is inhibition of proinflammatory type II IFN systemically or at the target organ. In multiple sclerosis (MS) and insulin-dependent diabetes mellitus (IDDM) at the target organ, and in rheumatoid arthritis (RA) as a regulator of other proinflammatory cytokines, IFN-gamma is the nexus of inflammation in autoimmunity. Ingested type I IFNs counteract type II IFN, overcome the relative lack of type I IFN activity, and ameliorate autoimmunity. The administration of type I IFNs (IFN-alpha/beta) via the gut offers an exciting alternative to systemic application for overcoming the type I IFN immunodeficiency in autoimmunity. Successful use of ingested type I IFN in three separate prototypical autoimmune diseases suggests a broad antiinflammatory therapeutic profile for this technology. |
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We have proposed a unifying hypothesis of the origin of autoimmunity as a type I IFN immunodeficiency syndrome involving inadequate regulation of the acquired immune system product IFN-gamma by the IFN-alpha/beta innate immune system. The common theme of ingested type I IFNs in autoimmunity is inhibition of proinflammatory type II IFN systemically or at the target organ. In multiple sclerosis (MS) and insulin-dependent diabetes mellitus (IDDM) at the target organ, and in rheumatoid arthritis (RA) as a regulator of other proinflammatory cytokines, IFN-gamma is the nexus of inflammation in autoimmunity. Ingested type I IFNs counteract type II IFN, overcome the relative lack of type I IFN activity, and ameliorate autoimmunity. The administration of type I IFNs (IFN-alpha/beta) via the gut offers an exciting alternative to systemic application for overcoming the type I IFN immunodeficiency in autoimmunity. Successful use of ingested type I IFN in three separate prototypical autoimmune diseases suggests a broad antiinflammatory therapeutic profile for this technology.</description><identifier>ISSN: 1079-9907</identifier><identifier>EISSN: 1557-7465</identifier><identifier>DOI: 10.1089/107999099313343</identifier><identifier>PMID: 10476927</identifier><language>eng</language><publisher>United States: Mary Ann Liebert, Inc</publisher><subject>Administration, Oral ; AIDS/HIV ; Autoimmunity ; Encephalomyelitis, Autoimmune, Experimental - immunology ; Humans ; Immunosuppression ; Interferon Type I - deficiency ; Intestinal Mucosa - immunology ; Lymphoid Tissue - immunology ; Multiple Sclerosis - immunology</subject><ispartof>Journal of interferon & cytokine research, 1999-08, Vol.19 (8), p.841-852</ispartof><rights>Copyright Mary Ann Liebert Inc. 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Successful use of ingested type I IFN in three separate prototypical autoimmune diseases suggests a broad antiinflammatory therapeutic profile for this technology.</description><subject>Administration, Oral</subject><subject>AIDS/HIV</subject><subject>Autoimmunity</subject><subject>Encephalomyelitis, Autoimmune, Experimental - immunology</subject><subject>Humans</subject><subject>Immunosuppression</subject><subject>Interferon Type I - deficiency</subject><subject>Intestinal Mucosa - immunology</subject><subject>Lymphoid Tissue - immunology</subject><subject>Multiple Sclerosis - immunology</subject><issn>1079-9907</issn><issn>1557-7465</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkTtPwzAUhS0EoqUwsyGLgS3Uj9iOx6qipVIFS5kj17kBV3kUO0HKv8dVO6AuTL7S-c6R7z0I3VPyTEmmp5QorTXRmlPOU36BxlQIlahUiss4RzWJshqhmxB2hBCZMX2NRpSkSmqmxqia9V3r6rpvXDdgF7DB3bAHvMKu6cCX4NsmKaB01kFjBxyGpvBtDdi23oPtoMDb6Gs-IRzmk3e1eMM_LkZ9AV7O1ptoi3J9i65KUwW4O70T9LF42cxfk_X7cjWfrRPLpOwSK1JemtJuLdCUlIwanglaCG4k5URYarktLSuEKQyTKQXDU5FxmkoFBuIhJujpmLv37Xcff5bXLlioKtNA24dcEUI1V9m_IFWcaS5VBB_PwF3b-yYukbN4cSIZIRGaHiHr2xA8lPneu9r4IackP9SVn9UVHQ-n2H5bQ_GHP_bDfwGCjI7g</recordid><startdate>199908</startdate><enddate>199908</enddate><creator>Brod, S A</creator><general>Mary Ann Liebert, 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>3V.</scope><scope>7QL</scope><scope>7T5</scope><scope>7T7</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</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>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</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>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>199908</creationdate><title>Autoimmunity is a type I interferon-deficiency syndrome corrected by ingested type I IFN via the GALT system</title><author>Brod, S A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c266t-c543fafcbce140f21a3851d53a61305c1c3cfc2d5ada2641ea345831467eae133</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Administration, Oral</topic><topic>AIDS/HIV</topic><topic>Autoimmunity</topic><topic>Encephalomyelitis, Autoimmune, Experimental - immunology</topic><topic>Humans</topic><topic>Immunosuppression</topic><topic>Interferon Type I - deficiency</topic><topic>Intestinal Mucosa - immunology</topic><topic>Lymphoid Tissue - immunology</topic><topic>Multiple Sclerosis - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Brod, S A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>PHMC-Proquest健康医学期刊库</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>Public Health Database (Proquest)</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)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</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>Biological Sciences</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest Science Journals</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</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>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - 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We have proposed a unifying hypothesis of the origin of autoimmunity as a type I IFN immunodeficiency syndrome involving inadequate regulation of the acquired immune system product IFN-gamma by the IFN-alpha/beta innate immune system. The common theme of ingested type I IFNs in autoimmunity is inhibition of proinflammatory type II IFN systemically or at the target organ. In multiple sclerosis (MS) and insulin-dependent diabetes mellitus (IDDM) at the target organ, and in rheumatoid arthritis (RA) as a regulator of other proinflammatory cytokines, IFN-gamma is the nexus of inflammation in autoimmunity. Ingested type I IFNs counteract type II IFN, overcome the relative lack of type I IFN activity, and ameliorate autoimmunity. The administration of type I IFNs (IFN-alpha/beta) via the gut offers an exciting alternative to systemic application for overcoming the type I IFN immunodeficiency in autoimmunity. Successful use of ingested type I IFN in three separate prototypical autoimmune diseases suggests a broad antiinflammatory therapeutic profile for this technology.</abstract><cop>United States</cop><pub>Mary Ann Liebert, Inc</pub><pmid>10476927</pmid><doi>10.1089/107999099313343</doi><tpages>12</tpages></addata></record> |
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subjects | Administration, Oral AIDS/HIV Autoimmunity Encephalomyelitis, Autoimmune, Experimental - immunology Humans Immunosuppression Interferon Type I - deficiency Intestinal Mucosa - immunology Lymphoid Tissue - immunology Multiple Sclerosis - immunology |
title | Autoimmunity is a type I interferon-deficiency syndrome corrected by ingested type I IFN via the GALT system |
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