T CELLS ARE CLEARLY THE ULTIMATE effectors of autoimmune (2009)
diabetes results from genetic defects manifest by
Mangada, Julie A., Pearson, Todd, Brehm, Michael A., Wicker, Linda S., Peterson, Laurence B., Shultz, Leonard D., ...
OBJECTIVE: NOD mice model human type 1 diabetes and are used to investigate tolerance induction protocols for islet transplantation in a setting of autoimmunity. However, costimulation blockade-based...
Serreze, David V., Osborne, Melissa A., Chen, Yi-Guang, Chapman, Harold D., Pearson, Todd, Brehm, Michael A., ...
In both humans and NOD mice, particular combinations of MHC genes provide the primary risk factor for development of the autoreactive T cell responses causing type 1 diabetes (T1D). Conversely, other...
Autoimmune diabetes and resistance to xenograft transplantation tolerance in NOD mice (2004)
Gordon, Ethel J., Wicker, Linda S., Peterson, Laurence B., Serreze, David V., Markees, Thomas G., Shultz, Leonard D., ...
Costimulation blockade induces prolonged rat islet and skin xenograft survival in C57BL/6 mice. Nonobese diabetic (NOD) mice, which are used to model human autoimmune diabetes, are resistant to...
Pearson, Todd, Weiser, Peter, Markees, Thomas G., Serreze, David V., Wicker, Linda S., Peterson, Laurence B., ...
NOD mice develop type 1 autoimmune diabetes and exhibit genetically dominant resistance to transplantation tolerance induction. These two phenotypes are genetically separable. Costimulation blockade...
Islet cell autoimmunity and transplantation tolerance: two distinct mechanisms (2003)
Pearson, Todd, Markees, Thomas G., Serreze, David V., Pierce, Melissa A., Wicker, Linda S., Peterson, Laurence B., ...
Recent advances in islet transplantation have enabled physicians to cure type 1 autoimmune diabetes, but at the cost of lifelong immunosuppression with its attendant side effects and long-term health...
Genetic separation of the transplantation tolerance and autoimmune phenotypes in NOD mice (2003)
Pearson, Todd, Markees, Thomas G., Serreze, David V., Pierce, Melissa A., Wicker, Linda S., Peterson, Laurence B., ...
Pearson, Todd, Markees, Thomas G., Serreze, David V., Pierce, Melissa A., Marron, Michele P., Wicker, Linda S., ...
Curing type 1 diabetes by islet transplantation requires overcoming both allorejection and recurrent autoimmunity. This has been achieved with systemic immunosuppression, but tolerance induction...
Pearson, Todd, Markees, Thomas G., Wicker, Linda S., Serreze, David V., Peterson, Laurence B., Mordes, John P., ...
The loss of self-tolerance leading to autoimmune type 1 diabetes in the NOD mouse model involves at least 19 genetic loci. In addition to their genetic defects in self-tolerance, NOD mice resist...
NOD mice have a generalized defect in their response to transplantation tolerance induction (1999)
Markees, Thomas G., Serreze, David V., Phillips, Nancy E., Sorli, Christopher H., Gordon, Ethel J., Shultz, Leonard D., ...
A protocol consisting of a single donor-specific transfusion (DST) plus a brief course of anti-CD154 monoclonal antibody (anti-CD40 ligand mAb) induces permanent islet allograft survival in...
Defects in limb, craniofacial, and thymic development in Jagged2 mutant mice (1998)
Jiang, Rulang, Lan, Yu, Chapman, Harry D., Shawber, Carrie, Norton, Christine R., Serreze, David V., ...
Mathews, Clayton E., Graser, Robert T., Savinov, Alexei, Serreze, David V., Leiter, Edward H.
Genetic analysis of autoimmune insulin-dependent diabetes mellitus (IDDM) has focused on genes controlling immune functions, with little investigation of innate susceptibility determinants expressed...
DiLorenzo, Teresa P., Graser, Robert T., Ono, Toshiro, Christianson, Gregory J., Chapman, Harold D., Roopenian, Derry C., ...
Nonobese diabetic (NOD) mice develop insulin-dependent diabetes mellitus due to autoimmune T lymphocyte-mediated destruction of pancreatic β cells. Although both major histocompatibility complex...
Hamilton-Williams, Emma E., Serreze, David V., Charlton, Brett, Johnson, Ellis A., Marron, Michele P., Müllbacher, Arno, ...
Type 1 diabetes in both humans and nonobese diabetic (NOD) mice results from T-cell-mediated autoimmune destruction of insulin-producing pancreatic β cells. Linkage studies have shown that type 1...
Marron, Michele P., Graser, Robert T., Chapman, Harold D., Serreze, David V.
Particular major histocompatibility complex (MHC) class II alleles clearly contribute to T cell-mediated autoimmune type 1 diabetes (T1D) in both humans and nonobese diabetic (NOD) mice. However,...
Lieberman, Scott M., Evans, Anne M., Han, Bingye, Takaki, Toshiyuki, Vinnitskaya, Yuliya, Caldwell, Jennifer A., ...
Type 1 diabetes is an autoimmune disease in which autoreactive T cells attack and destroy the insulin-producing pancreatic β cells. CD8+ T cells are essential for this β cell destruction, yet their...
Tracking autoimmune T cells in diabetes
Serreze, David V., Leiter, Edward H.
Insulin-dependent diabetes mellitus is usually caused by the autoimmune destruction of pancreatic β cells by T cells. Methodologies to track the development, migration, and functional activation of...
Defects in limb, craniofacial, and thymic development in Jagged2 mutant mice
Jiang, Rulang, Lan, Yu, Chapman, Harry D., Shawber, Carrie, Norton, Christine R., Serreze, David V., ...
The Notch signaling pathway is a conserved intercellular signaling mechanism that is essential for proper embryonic development in numerous metazoan organisms. We have examined the in vivo role of...
Serreze, David V., Wasserfall, Clive, Ottendorfer, Eric W., Stalvey, Michael, Pierce, Melissa A., Gauntt, Charles, ...
Type 1 diabetes acceleration in nonobese diabetic (NOD) mice through coxsackievirus B4 (CVB4) infection requires a preexisting critical mass of autoreactive T cells in pancreatic islets, and in the...
Pierce, Melissa A., Svetlanov, Anton, Horwitz, Marshall S., Serreze, David V.
The incidence of type 1 diabetes (T1D) is decreased in nonobese diabetic mice expressing the complete cassette of adenovirus early region 3 (E3) immunomodulating genes in pancreatic β cells....
Mathews, Clayton E., Graser, Robert T., Savinov, Alexei, Serreze, David V., Leiter, Edward H.
Genetic analysis of autoimmune insulin-dependent diabetes mellitus (IDDM) has focused on genes controlling immune functions, with little investigation of innate susceptibility determinants expressed...
DiLorenzo, Teresa P., Graser, Robert T., Ono, Toshiro, Christianson, Gregory J., Chapman, Harold D., Roopenian, Derry C., ...
Nonobese diabetic (NOD) mice develop insulin-dependent diabetes mellitus due to autoimmune T lymphocyte-mediated destruction of pancreatic β cells. Although both major histocompatibility complex...
Hamilton-Williams, Emma E., Serreze, David V., Charlton, Brett, Johnson, Ellis A., Marron, Michele P., Müllbacher, Arno, ...
Type 1 diabetes in both humans and nonobese diabetic (NOD) mice results from T-cell-mediated autoimmune destruction of insulin-producing pancreatic β cells. Linkage studies have shown that type 1...
Marron, Michele P., Graser, Robert T., Chapman, Harold D., Serreze, David V.
Particular major histocompatibility complex (MHC) class II alleles clearly contribute to T cell-mediated autoimmune type 1 diabetes (T1D) in both humans and nonobese diabetic (NOD) mice. However,...
Lieberman, Scott M., Evans, Anne M., Han, Bingye, Takaki, Toshiyuki, Vinnitskaya, Yuliya, Caldwell, Jennifer A., ...
Type 1 diabetes is an autoimmune disease in which autoreactive T cells attack and destroy the insulin-producing pancreatic β cells. CD8+ T cells are essential for this β cell destruction, yet their...
Tracking autoimmune T cells in diabetes
Serreze, David V., Leiter, Edward H.
Insulin-dependent diabetes mellitus is usually caused by the autoimmune destruction of pancreatic β cells by T cells. Methodologies to track the development, migration, and functional activation of...
Defects in limb, craniofacial, and thymic development in Jagged2 mutant mice
Jiang, Rulang, Lan, Yu, Chapman, Harry D., Shawber, Carrie, Norton, Christine R., Serreze, David V., ...
The Notch signaling pathway is a conserved intercellular signaling mechanism that is essential for proper embryonic development in numerous metazoan organisms. We have examined the in vivo role of...
Serreze, David V., Wasserfall, Clive, Ottendorfer, Eric W., Stalvey, Michael, Pierce, Melissa A., Gauntt, Charles, ...
Type 1 diabetes acceleration in nonobese diabetic (NOD) mice through coxsackievirus B4 (CVB4) infection requires a preexisting critical mass of autoreactive T cells in pancreatic islets, and in the...
Pierce, Melissa A., Svetlanov, Anton, Horwitz, Marshall S., Serreze, David V.
The incidence of type 1 diabetes (T1D) is decreased in nonobese diabetic mice expressing the complete cassette of adenovirus early region 3 (E3) immunomodulating genes in pancreatic β cells....
Fallarino, Francesca, Bianchi, Roberta, Orabona, Ciriana, Vacca, Carmine, Belladonna, Maria L., Fioretti, Maria C., ...
Prediabetes and diabetes in nonobese diabetic (NOD) mice have been targeted by a variety of immunotherapies, including the use of a soluble form of cytotoxic T lymphocyte antigen 4 (CTLA-4) and...
Mo, Jun-Song, Anderson, Michael G., Gregory, Meredith, Smith, Richard S., Savinova, Olga V., Serreze, David V., ...
Pigment dispersion syndrome causes iris pigment release and often progresses to elevated intraocular pressure and pigmentary glaucoma (PG). Because melanin pigment can have adjuvant like properties...
Mukhopadhaya, Arunika, Hanafusa, Tadashi, Jarchum, Irene, Chen, Yi-Guang, Iwai, Yoshiko, Serreze, David V., ...
Type 1 diabetes (T1D) is an autoimmune disease resulting from defects in central and peripheral tolerance and characterized by T cell-mediated destruction of islet β cells. Cytotoxic CD8+ T cells,...
Single domain antibodies: promising experimental and therapeutic tools in infection and immunity
Wesolowski, Janusz, Alzogaray, Vanina, Reyelt, Jan, Unger, Mandy, Juarez, Karla, Urrutia, Mariela, ...
Antibodies are important tools for experimental research and medical applications. Most antibodies are composed of two heavy and two light chains. Both chains contribute to the antigen-binding site...