Immunosuppressive potential of antimalarials
A hypothesis concerning the mechanism whereby chloroquine phosphate and hydrpxychloroquine sulfate are therapeutically active in rheumatoid arthritis is presented, based on in vitro data that (1) utilize drug concentrations not higher than those clinically achievable, and (2) might explain mechanism...
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| Veröffentlicht in: | The American journal of medicine 1983-07, Vol.75 (1), p.19-24 |
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| container_title | The American journal of medicine |
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| creator | Salmeron, G. Lipsky, P.E. |
| description | A hypothesis concerning the mechanism whereby chloroquine phosphate and hydrpxychloroquine sulfate are therapeutically active in rheumatoid arthritis is presented, based on in vitro data that (1) utilize drug concentrations not higher than those clinically achievable, and (2) might explain mechanisms that may be applicable in treated rheumatoid arthritis patients. Simple assay systems were used: normal human peripheral blood mononuclear cells were cultured, stimulated with various nonspecific agents, and assayed either for induction of T cell proliferation or generation of immunoglobulin-secreting cells. Results indicate that chloroquine inhibits tritiated thymidine in a dose-dependent way by interfering with the accessory function of monocytes, and that chloroquine inhibits the generation of immunoglobulin-secreting cells by selectively interfering with the secretion of Interleukin 1 by monocytes. |
| doi_str_mv | 10.1016/0002-9343(83)91266-4 |
| format | Article |
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Simple assay systems were used: normal human peripheral blood mononuclear cells were cultured, stimulated with various nonspecific agents, and assayed either for induction of T cell proliferation or generation of immunoglobulin-secreting cells. Results indicate that chloroquine inhibits tritiated thymidine in a dose-dependent way by interfering with the accessory function of monocytes, and that chloroquine inhibits the generation of immunoglobulin-secreting cells by selectively interfering with the secretion of Interleukin 1 by monocytes.</description><identifier>ISSN: 0002-9343</identifier><identifier>EISSN: 1555-7162</identifier><identifier>DOI: 10.1016/0002-9343(83)91266-4</identifier><identifier>PMID: 6603165</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Arthritis, Rheumatoid - drug therapy ; Arthritis, Rheumatoid - immunology ; Chloroquine - therapeutic use ; Humans ; Hydroxychloroquine - therapeutic use ; Immunoglobulins - immunology ; Immunosuppressive Agents ; Interleukin-1 - immunology ; Lymphocyte Activation - drug effects ; Monocytes - drug effects ; Monocytes - immunology ; T-Lymphocytes - drug effects</subject><ispartof>The American journal of medicine, 1983-07, Vol.75 (1), p.19-24</ispartof><rights>1983</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c272t-146850603e5efeabd84c64be5cc5cb22a33168a3f6fc2013956b1b423d919f853</citedby><cites>FETCH-LOGICAL-c272t-146850603e5efeabd84c64be5cc5cb22a33168a3f6fc2013956b1b423d919f853</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0002-9343(83)91266-4$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3541,27915,27916,45986</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/6603165$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Salmeron, G.</creatorcontrib><creatorcontrib>Lipsky, P.E.</creatorcontrib><title>Immunosuppressive potential of antimalarials</title><title>The American journal of medicine</title><addtitle>Am J Med</addtitle><description>A hypothesis concerning the mechanism whereby chloroquine phosphate and hydrpxychloroquine sulfate are therapeutically active in rheumatoid arthritis is presented, based on in vitro data that (1) utilize drug concentrations not higher than those clinically achievable, and (2) might explain mechanisms that may be applicable in treated rheumatoid arthritis patients. Simple assay systems were used: normal human peripheral blood mononuclear cells were cultured, stimulated with various nonspecific agents, and assayed either for induction of T cell proliferation or generation of immunoglobulin-secreting cells. Results indicate that chloroquine inhibits tritiated thymidine in a dose-dependent way by interfering with the accessory function of monocytes, and that chloroquine inhibits the generation of immunoglobulin-secreting cells by selectively interfering with the secretion of Interleukin 1 by monocytes.</description><subject>Arthritis, Rheumatoid - drug therapy</subject><subject>Arthritis, Rheumatoid - immunology</subject><subject>Chloroquine - therapeutic use</subject><subject>Humans</subject><subject>Hydroxychloroquine - therapeutic use</subject><subject>Immunoglobulins - immunology</subject><subject>Immunosuppressive Agents</subject><subject>Interleukin-1 - immunology</subject><subject>Lymphocyte Activation - drug effects</subject><subject>Monocytes - drug effects</subject><subject>Monocytes - immunology</subject><subject>T-Lymphocytes - drug effects</subject><issn>0002-9343</issn><issn>1555-7162</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1983</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1LAzEQhoMotVb_gUJPouBqvpu9CFL8KBS86DlksxOI7G7WZLfgvze1pUdPM8O8M-_Mg9AlwfcEE_mAMaZFyTi7Uey2JFTKgh-hKRFCFAsi6TGaHiSn6Cylr1ziUsgJmkiJGZFiiu5WbTt2IY19HyElv4F5HwboBm-aeXBzk7PWNCbmOp2jE5cDXOzjDH2-PH8s34r1--tq-bQuLF3QoSBcKoGzAwhwYKpacSt5BcJaYStKDcveyjAnnaWYsHxSRSpOWV2S0inBZuh6t7eP4XuENOjWJwtNYzoIY9IKCyEVJ1nId0IbQ0oRnO5jPjf-aIL1FpLeEtBbAlox_QdJ8zx2td8_Vi3Uh6E9ldx_3PUhP7nxEHWyHjoLtY9gB10H_7_BL0DodUE</recordid><startdate>19830718</startdate><enddate>19830718</enddate><creator>Salmeron, G.</creator><creator>Lipsky, P.E.</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>19830718</creationdate><title>Immunosuppressive potential of antimalarials</title><author>Salmeron, G. ; Lipsky, P.E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c272t-146850603e5efeabd84c64be5cc5cb22a33168a3f6fc2013956b1b423d919f853</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1983</creationdate><topic>Arthritis, Rheumatoid - drug therapy</topic><topic>Arthritis, Rheumatoid - immunology</topic><topic>Chloroquine - therapeutic use</topic><topic>Humans</topic><topic>Hydroxychloroquine - therapeutic use</topic><topic>Immunoglobulins - immunology</topic><topic>Immunosuppressive Agents</topic><topic>Interleukin-1 - immunology</topic><topic>Lymphocyte Activation - drug effects</topic><topic>Monocytes - drug effects</topic><topic>Monocytes - immunology</topic><topic>T-Lymphocytes - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Salmeron, G.</creatorcontrib><creatorcontrib>Lipsky, P.E.</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>The American journal of medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Salmeron, G.</au><au>Lipsky, P.E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Immunosuppressive potential of antimalarials</atitle><jtitle>The American journal of medicine</jtitle><addtitle>Am J Med</addtitle><date>1983-07-18</date><risdate>1983</risdate><volume>75</volume><issue>1</issue><spage>19</spage><epage>24</epage><pages>19-24</pages><issn>0002-9343</issn><eissn>1555-7162</eissn><abstract>A hypothesis concerning the mechanism whereby chloroquine phosphate and hydrpxychloroquine sulfate are therapeutically active in rheumatoid arthritis is presented, based on in vitro data that (1) utilize drug concentrations not higher than those clinically achievable, and (2) might explain mechanisms that may be applicable in treated rheumatoid arthritis patients. Simple assay systems were used: normal human peripheral blood mononuclear cells were cultured, stimulated with various nonspecific agents, and assayed either for induction of T cell proliferation or generation of immunoglobulin-secreting cells. Results indicate that chloroquine inhibits tritiated thymidine in a dose-dependent way by interfering with the accessory function of monocytes, and that chloroquine inhibits the generation of immunoglobulin-secreting cells by selectively interfering with the secretion of Interleukin 1 by monocytes.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>6603165</pmid><doi>10.1016/0002-9343(83)91266-4</doi><tpages>6</tpages></addata></record> |
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| ispartof | The American journal of medicine, 1983-07, Vol.75 (1), p.19-24 |
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| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals Complete |
| subjects | Arthritis, Rheumatoid - drug therapy Arthritis, Rheumatoid - immunology Chloroquine - therapeutic use Humans Hydroxychloroquine - therapeutic use Immunoglobulins - immunology Immunosuppressive Agents Interleukin-1 - immunology Lymphocyte Activation - drug effects Monocytes - drug effects Monocytes - immunology T-Lymphocytes - drug effects |
| title | Immunosuppressive potential of antimalarials |
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