Critical roles of CD30/CD30L interactions in Murine Autoimmune Diabetes
Chakrabarty, S., Nagata, M., Yasuda, H., Wen, L., Nakayama, M., Chowdhury, S.A., Yamada, K., Jin, Z., Kotani, R., Moriyama, H., Shimozato, O., Yagita, H., and Yokono, K. (2003) Critical roles of CD30/CD30L interactions in Murine Autoimmune Diabetes. Clinical and Experimental Immunology, 133 (3). pp. 318-325.
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CD30/CD30L is a member of tumour necrosis factor (TNF) receptor/TNF superfamily and has been implicated in immune-regulation. A genetic study has also suggested a possible implication of CD30 in spontaneous autoimmune diabetes in NOD mice. In this study, we investigated the involvement of CD30/CD30L in the development of diabetes in NOD mice. Flow cytometric analysis showed that CD30 and CD30L were highly expressed on CD4+ or CD8+ T cells in the spleen and pancreatic lymph node of younger NOD mice. In addition, islet-specific CD4+ or CD8+ T cell lines expressed CD30 and CD30L. Administration of a neutralizing anti-CD30L monoclonal antibody (mAb) from 2 to 10 week of age completely suppressed the development of spontaneous diabetes in NOD mice. In addition, the treatment with anti-CD30L mAb also inhibited the development of diabetes induced by adoptive transfer of spleen cells from diabetic NOD mice or islet-specific CD4+ or CD8+ T cell lines into NOD-SCID mice. Furthermore, anti-CD30L mAb inhibited T cell proliferation in response to islet antigens. These results suggested that CD30/CD30L interaction plays important roles in both induction and effector phases of autoimmune diabetes in NOD mice.
Copyright 2003 Blackwell Publishing. The definitive version is available at www.blackwell-synergy.com
|Keywords:||Immunotherapy, Monoclonal antibody, NOD mouse, TNF superfamily, Type 1 Diabetes|
|FoR Codes:||11 MEDICAL AND HEALTH SCIENCES > 1107 Immunology > 110703 Autoimmunity @ 0%|
|Deposited On:||01 Nov 2006|
|Last Modified:||14 Feb 2011 00:55|
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