Abstract
Summary: The non-obese diabetic (NOD) mouse model of autoimmune (type 1) diabetes has contributed greatly to our understanding of disease pathogenesis and has facilitated the development and testing of therapeutic strategies to combat the disease. Although the model is a valuable immunological tool in its own right, it reaches its fullest potential in areas where its findings translate to the human disease. Perhaps the foremost example of this is the field of T-cell antigen discovery, from which diverse benefits can be derived, including the development of antigen-specific disease interventions. The majority of NOD T-cell antigens are also targets of T-cell autoimmunity in patients with type 1 diabetes, and several of these are currently being evaluated in clinical trials. Here we review the journeys of these antigens from bench to bedside. We also discuss several recently identified NOD T-cell autoantigens whose translational potential warrants further investigation.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 459-465 |
| Number of pages | 7 |
| Journal | Immunology |
| Volume | 131 |
| Issue number | 4 |
| DOIs | |
| State | Published - Dec 2010 |
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Keywords
- Autoantigens
- Autoimmune diabetes
- Non-obese diabetic mice
- Therapies
- Type 1 diabetes
ASJC Scopus subject areas
- Immunology
- Immunology and Allergy
Cite this
T-cell autoantigens in the non-obese diabetic mouse model of autoimmune diabetes. / Babad, Jeffrey; Geliebter, Ari; DiLorenzo, Teresa P.
In: Immunology, Vol. 131, No. 4, 12.2010, p. 459-465.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - T-cell autoantigens in the non-obese diabetic mouse model of autoimmune diabetes
AU - Babad, Jeffrey
AU - Geliebter, Ari
AU - DiLorenzo, Teresa P.
PY - 2010/12
Y1 - 2010/12
N2 - Summary: The non-obese diabetic (NOD) mouse model of autoimmune (type 1) diabetes has contributed greatly to our understanding of disease pathogenesis and has facilitated the development and testing of therapeutic strategies to combat the disease. Although the model is a valuable immunological tool in its own right, it reaches its fullest potential in areas where its findings translate to the human disease. Perhaps the foremost example of this is the field of T-cell antigen discovery, from which diverse benefits can be derived, including the development of antigen-specific disease interventions. The majority of NOD T-cell antigens are also targets of T-cell autoimmunity in patients with type 1 diabetes, and several of these are currently being evaluated in clinical trials. Here we review the journeys of these antigens from bench to bedside. We also discuss several recently identified NOD T-cell autoantigens whose translational potential warrants further investigation.
AB - Summary: The non-obese diabetic (NOD) mouse model of autoimmune (type 1) diabetes has contributed greatly to our understanding of disease pathogenesis and has facilitated the development and testing of therapeutic strategies to combat the disease. Although the model is a valuable immunological tool in its own right, it reaches its fullest potential in areas where its findings translate to the human disease. Perhaps the foremost example of this is the field of T-cell antigen discovery, from which diverse benefits can be derived, including the development of antigen-specific disease interventions. The majority of NOD T-cell antigens are also targets of T-cell autoimmunity in patients with type 1 diabetes, and several of these are currently being evaluated in clinical trials. Here we review the journeys of these antigens from bench to bedside. We also discuss several recently identified NOD T-cell autoantigens whose translational potential warrants further investigation.
KW - Autoantigens
KW - Autoimmune diabetes
KW - Non-obese diabetic mice
KW - Therapies
KW - Type 1 diabetes
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UR - http://www.scopus.com/inward/citedby.url?scp=78149375691&partnerID=8YFLogxK
U2 - 10.1111/j.1365-2567.2010.03362.x
DO - 10.1111/j.1365-2567.2010.03362.x
M3 - Article
C2 - 21039471
AN - SCOPUS:78149375691
VL - 131
SP - 459
EP - 465
JO - Immunology
JF - Immunology
SN - 0019-2805
IS - 4
ER -