Cargando…
T-Cell Promiscuity in Autoimmune Diabetes
OBJECTIVE—It is well established that the primary mediators of β-cell destruction in type 1 diabetes are T-cells. Nevertheless, the molecular basis for recognition of β-cell–specific epitopes by pathogenic T-cells remains ill defined; we seek to further explore this issue. RESEARCH DESIGN AND METHOD...
Autores principales: | Li, Li, Wang, Bo, Frelinger, Jeffrey A., Tisch, Roland |
---|---|
Formato: | Texto |
Lenguaje: | English |
Publicado: |
American Diabetes Association
2008
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2494676/ https://www.ncbi.nlm.nih.gov/pubmed/18492786 http://dx.doi.org/10.2337/db08-0383 |
Ejemplares similares
-
Long-Term Remission of Diabetes in NOD Mice Is Induced by Nondepleting Anti-CD4 and Anti-CD8 Antibodies
por: Yi, Zuoan, et al.
Publicado: (2012) -
Targeting CD22 Reprograms B-Cells and Reverses Autoimmune Diabetes
por: Fiorina, Paolo, et al.
Publicado: (2008) -
Prevention of Autoimmune Diabetes by Ectopic Pancreatic β-Cell Expression of Interleukin-35
por: Bettini, Maria, et al.
Publicado: (2012) -
HLA-A2–Matched Peripheral Blood Mononuclear Cells From Type 1 Diabetic Patients, but Not Nondiabetic Donors, Transfer Insulitis to NOD-scid/γc(null)/HLA-A2 Transgenic Mice Concurrent With the Expansion of Islet-Specific CD8(+) T cells
por: Whitfield-Larry, Fatima, et al.
Publicado: (2011) -
Deficiency of Nuclear Factor-κB c-Rel Accelerates the Development of Autoimmune Diabetes in NOD Mice
por: Ramakrishnan, Parameswaran, et al.
Publicado: (2016)