期刊
JOURNAL OF AUTOIMMUNITY
卷 34, 期 4, 页码 478-484出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.jaut.2009.12.008
关键词
Gamma delta T cells; T cell receptor; Insulin; Autoreactivity; Autoimmune diabetes
类别
资金
- National Institutes of Health [R01DK55969]
- NIH Autoimmunity Prevention Center [2U19A1050864]
- National Institute of Diabetes and Digestive and Kidney Diseases [P30 DK57516]
- American Diabetes Association
- Juvenile Diabetes Foundation [1-2006-16, 4-2007-1056, 3-2008-107]
- NIH Autoimmunity Center Pilot Project
- ADA [7-06-MN-17]
- [K99 DK080885]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL065410] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R00DK080885] Funding Source: NIH RePORTER
The range and physical qualities of molecules that act as ligands for the gamma delta T cell receptors (TCRs) remain uncertain. Processed insulin is recognized by alpha beta T cells, which mediate diabetes in non-obese diabetic (NOD) mice. Here, we present evidence that gamma delta T cells in these mice recognize processed insulin as well. Hybridomas generated from NOD spleen and pancreatic lymph nodes included clones expressing gamma delta TCRs that responded specifically to purified islets of Langerhans and to an insulin peptide, but not to intact insulin. The gamma delta TCRs associated with this type of response are diverse, but a cloned gamma delta TCR was sufficient to transfer the response. The response to the insulin peptide was autonomous as demonstrated by stimulating single responder cells in isolation. This study reveals a novel specificity for gamma delta TCRs, and raises the possibility that gamma delta T cells become involved in islet-specific autoimmunity. (C) 2009 Elsevier Ltd. All rights reserved.
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