Thyroid-Stimulating Monoclonal Antibodies
Thyrotropin (TSH) receptor monoclonal antibodies (TSHR mAbs) were obtained from cDNA-immunized NMRI mice. Three mAb immunoglobulin Gs (IgGs) (TSmAbs 1-3) that had distinct V H and V L region sequences stimulated cyclic adenosine monophosphate (cAMP) production in isolated porcine thyroid cells great...
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| Veröffentlicht in: | Thyroid (New York, N.Y.) N.Y.), 2002-12, Vol.12 (12), p.143-1050 |
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| creator | Sanders, Jane Jeffreys, Jennifer Depraetere, Hilde Richards, Tonya Evans, Michele Kiddie, Angela Brereton, Karen Groenen, Marleen Oda, Yasuo Furmaniak, Jadwiga Rees Smith, Bernard |
| description | Thyrotropin (TSH) receptor monoclonal antibodies (TSHR mAbs) were obtained from cDNA-immunized NMRI mice. Three mAb immunoglobulin Gs (IgGs) (TSmAbs 1-3) that had distinct V
H
and V
L
region sequences stimulated cyclic adenosine monophosphate (cAMP) production in isolated porcine thyroid cells greater than 10× basal and as little as 20 ng/mL (0.13 nmol/L) of TSmAb 1 IgG caused
a 2× basal stimulation. TSmAb 1 and 2 Fab fragments were also effective stimulators and thyroid-stimulating activities of the IgGs and Fabs were confirmed using TSHR transfected Chinese hamster ovary
(CHO) cells. The TSmAbs also inhibited
125
I-labeled TSH binding to TSHR-coated tubes by 50% or more at concentrations of 1 μg/mL or less and gave 15%-20% inhibition at 20-50 ng/mL.
125
I-labeled
TSmAbs bound to TSHR-coated tubes with high affinity (~10
10
L/mol) and this binding was inhibited by TSHR autoantibodies with both TSH agonist and antagonist activities. Inhibition of labeled
TSmAb binding by Graves' sera correlated well with inhibition of TSH binding (
r
= 0.96;
n
= 18;
p
< 0.001 for TSmAb 2). The TSmAbs have considerable potential as (1) new probes for
TSHR structure-function studies, (2) reagents for new assays for TSHR autoantibodies, and (3) alternatives to recombinant TSH in various
in vivo
applications. |
| doi_str_mv | 10.1089/105072502321085135 |
| format | Article |
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H
and V
L
region sequences stimulated cyclic adenosine monophosphate (cAMP) production in isolated porcine thyroid cells greater than 10× basal and as little as 20 ng/mL (0.13 nmol/L) of TSmAb 1 IgG caused
a 2× basal stimulation. TSmAb 1 and 2 Fab fragments were also effective stimulators and thyroid-stimulating activities of the IgGs and Fabs were confirmed using TSHR transfected Chinese hamster ovary
(CHO) cells. The TSmAbs also inhibited
125
I-labeled TSH binding to TSHR-coated tubes by 50% or more at concentrations of 1 μg/mL or less and gave 15%-20% inhibition at 20-50 ng/mL.
125
I-labeled
TSmAbs bound to TSHR-coated tubes with high affinity (~10
10
L/mol) and this binding was inhibited by TSHR autoantibodies with both TSH agonist and antagonist activities. Inhibition of labeled
TSmAb binding by Graves' sera correlated well with inhibition of TSH binding (
r
= 0.96;
n
= 18;
p
< 0.001 for TSmAb 2). The TSmAbs have considerable potential as (1) new probes for
TSHR structure-function studies, (2) reagents for new assays for TSHR autoantibodies, and (3) alternatives to recombinant TSH in various
in vivo
applications.</description><identifier>ISSN: 1050-7256</identifier><identifier>EISSN: 1557-9077</identifier><identifier>DOI: 10.1089/105072502321085135</identifier><identifier>PMID: 12593717</identifier><language>eng</language><publisher>United States: Mary Ann Liebert, Inc</publisher><subject>Animals ; Animals, Outbred Strains ; Antibodies, Monoclonal - immunology ; Antibodies, Monoclonal - pharmacology ; Autoantibodies - immunology ; Autoantibodies - pharmacology ; Binding, Competitive - immunology ; CHO Cells ; Cricetinae ; Graves Disease - immunology ; Humans ; Immunization ; Iodine Radioisotopes ; Laboratory Research Papers ; Mice ; Receptors, Thyrotropin - immunology ; Receptors, Thyrotropin - metabolism ; Thyroid Gland - immunology ; Thyrotropin - metabolism ; Thyrotropin - pharmacology</subject><ispartof>Thyroid (New York, N.Y.), 2002-12, Vol.12 (12), p.143-1050</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c350t-e80640d9a9b3075e9b82bd6edcfd3dbeffdf617ce16d3ce7d2a17b824ccaa1e43</citedby><cites>FETCH-LOGICAL-c350t-e80640d9a9b3075e9b82bd6edcfd3dbeffdf617ce16d3ce7d2a17b824ccaa1e43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.liebertpub.com/doi/epdf/10.1089/105072502321085135$$EPDF$$P50$$Gmaryannliebert$$H</linktopdf><linktohtml>$$Uhttps://www.liebertpub.com/doi/full/10.1089/105072502321085135$$EHTML$$P50$$Gmaryannliebert$$H</linktohtml><link.rule.ids>315,781,785,3043,21728,27929,27930,55296,55308</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12593717$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sanders, Jane</creatorcontrib><creatorcontrib>Jeffreys, Jennifer</creatorcontrib><creatorcontrib>Depraetere, Hilde</creatorcontrib><creatorcontrib>Richards, Tonya</creatorcontrib><creatorcontrib>Evans, Michele</creatorcontrib><creatorcontrib>Kiddie, Angela</creatorcontrib><creatorcontrib>Brereton, Karen</creatorcontrib><creatorcontrib>Groenen, Marleen</creatorcontrib><creatorcontrib>Oda, Yasuo</creatorcontrib><creatorcontrib>Furmaniak, Jadwiga</creatorcontrib><creatorcontrib>Rees Smith, Bernard</creatorcontrib><title>Thyroid-Stimulating Monoclonal Antibodies</title><title>Thyroid (New York, N.Y.)</title><addtitle>Thyroid</addtitle><description>Thyrotropin (TSH) receptor monoclonal antibodies (TSHR mAbs) were obtained from cDNA-immunized NMRI mice. Three mAb immunoglobulin Gs (IgGs) (TSmAbs 1-3) that had distinct V
H
and V
L
region sequences stimulated cyclic adenosine monophosphate (cAMP) production in isolated porcine thyroid cells greater than 10× basal and as little as 20 ng/mL (0.13 nmol/L) of TSmAb 1 IgG caused
a 2× basal stimulation. TSmAb 1 and 2 Fab fragments were also effective stimulators and thyroid-stimulating activities of the IgGs and Fabs were confirmed using TSHR transfected Chinese hamster ovary
(CHO) cells. The TSmAbs also inhibited
125
I-labeled TSH binding to TSHR-coated tubes by 50% or more at concentrations of 1 μg/mL or less and gave 15%-20% inhibition at 20-50 ng/mL.
125
I-labeled
TSmAbs bound to TSHR-coated tubes with high affinity (~10
10
L/mol) and this binding was inhibited by TSHR autoantibodies with both TSH agonist and antagonist activities. Inhibition of labeled
TSmAb binding by Graves' sera correlated well with inhibition of TSH binding (
r
= 0.96;
n
= 18;
p
< 0.001 for TSmAb 2). The TSmAbs have considerable potential as (1) new probes for
TSHR structure-function studies, (2) reagents for new assays for TSHR autoantibodies, and (3) alternatives to recombinant TSH in various
in vivo
applications.</description><subject>Animals</subject><subject>Animals, Outbred Strains</subject><subject>Antibodies, Monoclonal - immunology</subject><subject>Antibodies, Monoclonal - pharmacology</subject><subject>Autoantibodies - immunology</subject><subject>Autoantibodies - pharmacology</subject><subject>Binding, Competitive - immunology</subject><subject>CHO Cells</subject><subject>Cricetinae</subject><subject>Graves Disease - immunology</subject><subject>Humans</subject><subject>Immunization</subject><subject>Iodine Radioisotopes</subject><subject>Laboratory Research Papers</subject><subject>Mice</subject><subject>Receptors, Thyrotropin - immunology</subject><subject>Receptors, Thyrotropin - metabolism</subject><subject>Thyroid Gland - immunology</subject><subject>Thyrotropin - metabolism</subject><subject>Thyrotropin - pharmacology</subject><issn>1050-7256</issn><issn>1557-9077</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkDtPwzAYRS0EoqXwBxhQJySGgB-1nYxVxUsqYqDMkR9fwMiJi50M_fc4aiUGFqbvoXPPcBG6JPiW4LK6I5hjSTmmjOabE8aP0JRwLosKS3mc9wwUmRATdJbSF8ZElJKdogmhvGKSyCm62XzuYnC2eOtdO3jVu-5j_hK6YHzolJ8vu97pYB2kc3TSKJ_g4jBn6P3hfrN6Ktavj8-r5bowjOO-gBKLBbaVqjTDkkOlS6qtAGsay6yGprGNINIAEZYZkJYqIjOzMEYpAgs2Q9d77zaG7wFSX7cuGfBedRCGVEtaci7kCNI9aGJIKUJTb6NrVdzVBNdjQfXfgnLo6mAfdAv2N3JoJAPlHhjfquu8Aw2x_4_7B_SscgM</recordid><startdate>20021201</startdate><enddate>20021201</enddate><creator>Sanders, Jane</creator><creator>Jeffreys, Jennifer</creator><creator>Depraetere, Hilde</creator><creator>Richards, Tonya</creator><creator>Evans, Michele</creator><creator>Kiddie, Angela</creator><creator>Brereton, Karen</creator><creator>Groenen, Marleen</creator><creator>Oda, Yasuo</creator><creator>Furmaniak, Jadwiga</creator><creator>Rees Smith, Bernard</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>7X8</scope></search><sort><creationdate>20021201</creationdate><title>Thyroid-Stimulating Monoclonal Antibodies</title><author>Sanders, Jane ; Jeffreys, Jennifer ; Depraetere, Hilde ; Richards, Tonya ; Evans, Michele ; Kiddie, Angela ; Brereton, Karen ; Groenen, Marleen ; Oda, Yasuo ; Furmaniak, Jadwiga ; Rees Smith, Bernard</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c350t-e80640d9a9b3075e9b82bd6edcfd3dbeffdf617ce16d3ce7d2a17b824ccaa1e43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Animals</topic><topic>Animals, Outbred Strains</topic><topic>Antibodies, Monoclonal - immunology</topic><topic>Antibodies, Monoclonal - pharmacology</topic><topic>Autoantibodies - immunology</topic><topic>Autoantibodies - pharmacology</topic><topic>Binding, Competitive - immunology</topic><topic>CHO Cells</topic><topic>Cricetinae</topic><topic>Graves Disease - immunology</topic><topic>Humans</topic><topic>Immunization</topic><topic>Iodine Radioisotopes</topic><topic>Laboratory Research Papers</topic><topic>Mice</topic><topic>Receptors, Thyrotropin - immunology</topic><topic>Receptors, Thyrotropin - metabolism</topic><topic>Thyroid Gland - immunology</topic><topic>Thyrotropin - metabolism</topic><topic>Thyrotropin - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sanders, Jane</creatorcontrib><creatorcontrib>Jeffreys, Jennifer</creatorcontrib><creatorcontrib>Depraetere, Hilde</creatorcontrib><creatorcontrib>Richards, Tonya</creatorcontrib><creatorcontrib>Evans, Michele</creatorcontrib><creatorcontrib>Kiddie, Angela</creatorcontrib><creatorcontrib>Brereton, Karen</creatorcontrib><creatorcontrib>Groenen, Marleen</creatorcontrib><creatorcontrib>Oda, Yasuo</creatorcontrib><creatorcontrib>Furmaniak, Jadwiga</creatorcontrib><creatorcontrib>Rees Smith, Bernard</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>Thyroid (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sanders, Jane</au><au>Jeffreys, Jennifer</au><au>Depraetere, Hilde</au><au>Richards, Tonya</au><au>Evans, Michele</au><au>Kiddie, Angela</au><au>Brereton, Karen</au><au>Groenen, Marleen</au><au>Oda, Yasuo</au><au>Furmaniak, Jadwiga</au><au>Rees Smith, Bernard</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Thyroid-Stimulating Monoclonal Antibodies</atitle><jtitle>Thyroid (New York, N.Y.)</jtitle><addtitle>Thyroid</addtitle><date>2002-12-01</date><risdate>2002</risdate><volume>12</volume><issue>12</issue><spage>143</spage><epage>1050</epage><pages>143-1050</pages><issn>1050-7256</issn><eissn>1557-9077</eissn><abstract>Thyrotropin (TSH) receptor monoclonal antibodies (TSHR mAbs) were obtained from cDNA-immunized NMRI mice. Three mAb immunoglobulin Gs (IgGs) (TSmAbs 1-3) that had distinct V
H
and V
L
region sequences stimulated cyclic adenosine monophosphate (cAMP) production in isolated porcine thyroid cells greater than 10× basal and as little as 20 ng/mL (0.13 nmol/L) of TSmAb 1 IgG caused
a 2× basal stimulation. TSmAb 1 and 2 Fab fragments were also effective stimulators and thyroid-stimulating activities of the IgGs and Fabs were confirmed using TSHR transfected Chinese hamster ovary
(CHO) cells. The TSmAbs also inhibited
125
I-labeled TSH binding to TSHR-coated tubes by 50% or more at concentrations of 1 μg/mL or less and gave 15%-20% inhibition at 20-50 ng/mL.
125
I-labeled
TSmAbs bound to TSHR-coated tubes with high affinity (~10
10
L/mol) and this binding was inhibited by TSHR autoantibodies with both TSH agonist and antagonist activities. Inhibition of labeled
TSmAb binding by Graves' sera correlated well with inhibition of TSH binding (
r
= 0.96;
n
= 18;
p
< 0.001 for TSmAb 2). The TSmAbs have considerable potential as (1) new probes for
TSHR structure-function studies, (2) reagents for new assays for TSHR autoantibodies, and (3) alternatives to recombinant TSH in various
in vivo
applications.</abstract><cop>United States</cop><pub>Mary Ann Liebert, Inc</pub><pmid>12593717</pmid><doi>10.1089/105072502321085135</doi><tpages>908</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1050-7256 |
| ispartof | Thyroid (New York, N.Y.), 2002-12, Vol.12 (12), p.143-1050 |
| issn | 1050-7256 1557-9077 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_72855674 |
| source | Mary Ann Liebert Online Subscription; MEDLINE |
| subjects | Animals Animals, Outbred Strains Antibodies, Monoclonal - immunology Antibodies, Monoclonal - pharmacology Autoantibodies - immunology Autoantibodies - pharmacology Binding, Competitive - immunology CHO Cells Cricetinae Graves Disease - immunology Humans Immunization Iodine Radioisotopes Laboratory Research Papers Mice Receptors, Thyrotropin - immunology Receptors, Thyrotropin - metabolism Thyroid Gland - immunology Thyrotropin - metabolism Thyrotropin - pharmacology |
| title | Thyroid-Stimulating Monoclonal Antibodies |
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