Absence of lymph nodes in NOD mice treated with Lymphotoxin-[beta] receptor immunoglobulin protects from diabetes
Pregnant nonobese diabetic (NOD) mice were treated with lymphotoxin-[beta] receptor immunoglobulin fusion protein (LT[beta]R-Ig) or control human immunoglobulin on days embryonic day 11 (E11) and E14, and offspring were followed for the development of anti-[beta]-cell antibodies, islet pathology, an...
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| Veröffentlicht in: | Diabetes (New York, N.Y.) N.Y.), 2004-12, Vol.53 (12), p.3115 |
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| creator | Levisetti, Matteo G Suri, Anish Frederick, Katherine Unanue, Emil R |
| description | Pregnant nonobese diabetic (NOD) mice were treated with lymphotoxin-[beta] receptor immunoglobulin fusion protein (LT[beta]R-Ig) or control human immunoglobulin on days embryonic day 11 (E11) and E14, and offspring were followed for the development of anti-[beta]-cell antibodies, islet pathology, and hyperglycemia. The development of anti-[beta]-cell surface antibodies was abrogated in treated mice compared with controls. Autopsy examination of the mice at 30 weeks of age revealed normal development of secondary lymphoid structures in the control animals; however, mice treated with LT[beta]R-Ig had no axillary, inguinal, popliteal, or peripancreatic lymph nodes. Histological examination of the pancreata of the control mice revealed a severe and destructive mononuclear cellular infiltrate in the islets, whereas the islets of the LT[beta]R-Ig-treated mice were devoid of any insulitis. None of the LT[beta]R-Ig-treated mice (n = 22) developed diabetes; in contrast, 80% of the control mice (n = 46) developed diabetes at 1 year of age. The LT[beta]R-Ig-treated mice did not contain diabetogenic T-cells. However, the treated mice developed diabetes upon inoculation with diabetogenic T-cells. In this model of spontaneous autoimmune diabetes, secondary lymphoid structures, most likely the peripancreatic lymph nodes, were essential for the development of pathologic anti-[beta]-cell autoimmunity. |
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The development of anti-[beta]-cell surface antibodies was abrogated in treated mice compared with controls. Autopsy examination of the mice at 30 weeks of age revealed normal development of secondary lymphoid structures in the control animals; however, mice treated with LT[beta]R-Ig had no axillary, inguinal, popliteal, or peripancreatic lymph nodes. Histological examination of the pancreata of the control mice revealed a severe and destructive mononuclear cellular infiltrate in the islets, whereas the islets of the LT[beta]R-Ig-treated mice were devoid of any insulitis. None of the LT[beta]R-Ig-treated mice (n = 22) developed diabetes; in contrast, 80% of the control mice (n = 46) developed diabetes at 1 year of age. The LT[beta]R-Ig-treated mice did not contain diabetogenic T-cells. However, the treated mice developed diabetes upon inoculation with diabetogenic T-cells. In this model of spontaneous autoimmune diabetes, secondary lymphoid structures, most likely the peripancreatic lymph nodes, were essential for the development of pathologic anti-[beta]-cell autoimmunity.</description><identifier>ISSN: 0012-1797</identifier><identifier>EISSN: 1939-327X</identifier><identifier>CODEN: DIAEAZ</identifier><language>eng</language><publisher>New York: American Diabetes Association</publisher><subject>Antibodies ; Arthritis ; Autoimmune diseases ; Care and treatment ; Dendritic cells ; Diabetes ; Diabetes research ; Immunoglobulins ; Laboratory animals ; Lymph nodes ; Lymphatic system ; Pathogenesis ; Proteins</subject><ispartof>Diabetes (New York, N.Y.), 2004-12, Vol.53 (12), p.3115</ispartof><rights>COPYRIGHT 2004 American Diabetes Association</rights><rights>Copyright American Diabetes Association Dec 2004</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids></links><search><creatorcontrib>Levisetti, Matteo G</creatorcontrib><creatorcontrib>Suri, Anish</creatorcontrib><creatorcontrib>Frederick, Katherine</creatorcontrib><creatorcontrib>Unanue, Emil R</creatorcontrib><title>Absence of lymph nodes in NOD mice treated with Lymphotoxin-[beta] receptor immunoglobulin protects from diabetes</title><title>Diabetes (New York, N.Y.)</title><addtitle>Diabetes</addtitle><description>Pregnant nonobese diabetic (NOD) mice were treated with lymphotoxin-[beta] receptor immunoglobulin fusion protein (LT[beta]R-Ig) or control human immunoglobulin on days embryonic day 11 (E11) and E14, and offspring were followed for the development of anti-[beta]-cell antibodies, islet pathology, and hyperglycemia. The development of anti-[beta]-cell surface antibodies was abrogated in treated mice compared with controls. Autopsy examination of the mice at 30 weeks of age revealed normal development of secondary lymphoid structures in the control animals; however, mice treated with LT[beta]R-Ig had no axillary, inguinal, popliteal, or peripancreatic lymph nodes. Histological examination of the pancreata of the control mice revealed a severe and destructive mononuclear cellular infiltrate in the islets, whereas the islets of the LT[beta]R-Ig-treated mice were devoid of any insulitis. None of the LT[beta]R-Ig-treated mice (n = 22) developed diabetes; in contrast, 80% of the control mice (n = 46) developed diabetes at 1 year of age. The LT[beta]R-Ig-treated mice did not contain diabetogenic T-cells. However, the treated mice developed diabetes upon inoculation with diabetogenic T-cells. In this model of spontaneous autoimmune diabetes, secondary lymphoid structures, most likely the peripancreatic lymph nodes, were essential for the development of pathologic anti-[beta]-cell autoimmunity.</description><subject>Antibodies</subject><subject>Arthritis</subject><subject>Autoimmune diseases</subject><subject>Care and treatment</subject><subject>Dendritic cells</subject><subject>Diabetes</subject><subject>Diabetes research</subject><subject>Immunoglobulins</subject><subject>Laboratory animals</subject><subject>Lymph nodes</subject><subject>Lymphatic system</subject><subject>Pathogenesis</subject><subject>Proteins</subject><issn>0012-1797</issn><issn>1939-327X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNotjk1LxDAYhIsouK7-h-A9kKRN0hyX9RMW96AHQaSk6ZtulzTZbVJc_70RZQ5zmIeZOSsWVJUKl0y-nxcLQijDVCp5WVzFuCeEiKxFcVy1EbwBFCxy3-Nhh3zoIKLBo5ftHRqHHKUJdIIOfQ1phza_UEjhNHj80ULSn2gCA4cUJjSM4-xD70I7u1xwmEICkyKyUxhRN-iMQ7wuLqx2EW7-fVm8Pty_rZ_wZvv4vF5tcC84x6WyvNJUd4xTSqzlQvLSCGmkoqy2XLa1JC0IxeuaWqKV6AxQrpmuLGhRLovbv9Z84jhDTM0-zJPPgw2jopI1qXiG8B_UawfN4E3wCU7JBOeghybfWW-bFWWCskoRUv4AlthmlA</recordid><startdate>20041201</startdate><enddate>20041201</enddate><creator>Levisetti, Matteo G</creator><creator>Suri, Anish</creator><creator>Frederick, Katherine</creator><creator>Unanue, Emil R</creator><general>American Diabetes Association</general><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</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>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M2P</scope><scope>M7P</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>S0X</scope></search><sort><creationdate>20041201</creationdate><title>Absence of lymph nodes in NOD mice treated with Lymphotoxin-[beta] receptor immunoglobulin protects from diabetes</title><author>Levisetti, Matteo G ; 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The development of anti-[beta]-cell surface antibodies was abrogated in treated mice compared with controls. Autopsy examination of the mice at 30 weeks of age revealed normal development of secondary lymphoid structures in the control animals; however, mice treated with LT[beta]R-Ig had no axillary, inguinal, popliteal, or peripancreatic lymph nodes. Histological examination of the pancreata of the control mice revealed a severe and destructive mononuclear cellular infiltrate in the islets, whereas the islets of the LT[beta]R-Ig-treated mice were devoid of any insulitis. None of the LT[beta]R-Ig-treated mice (n = 22) developed diabetes; in contrast, 80% of the control mice (n = 46) developed diabetes at 1 year of age. The LT[beta]R-Ig-treated mice did not contain diabetogenic T-cells. However, the treated mice developed diabetes upon inoculation with diabetogenic T-cells. In this model of spontaneous autoimmune diabetes, secondary lymphoid structures, most likely the peripancreatic lymph nodes, were essential for the development of pathologic anti-[beta]-cell autoimmunity.</abstract><cop>New York</cop><pub>American Diabetes Association</pub></addata></record> |
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| subjects | Antibodies Arthritis Autoimmune diseases Care and treatment Dendritic cells Diabetes Diabetes research Immunoglobulins Laboratory animals Lymph nodes Lymphatic system Pathogenesis Proteins |
| title | Absence of lymph nodes in NOD mice treated with Lymphotoxin-[beta] receptor immunoglobulin protects from diabetes |
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