Defective suppressor function in CD4(+)CD25(+) T-cells from patients with type 1 diabetes.
By Shelley Lindley, C. Dayan, A. Bishop, B. Roep, M. Peakman, T. Tree. Diabetes, 2005
885 citations recorded by the source corpus.
Subfields: Endocrinology, Diabetes and Metabolism, Genetics, Surgery
View Paper: https://www.semanticscholar.org/paper/2a23d913bbbbcb714496dbec8485c59509b96e92
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
- Loise M. Francisco
- M. Battaglia
- P. Sage
- A. Stabilini
- B. Migliavacca
- Arlene H. Sharpe
- J. Horejs-Hoeck
- T. Kaupper
Citations in the corpus
- Central role of defective interleukin-2 production in the triggering of islet autoimmune destruction. (2008, neutral): “Studies of Treg cell dynamics in human T1D patients have produced disparate results, ranging from reduced Treg cell frequency (Kukreja et al., 2002) or function (Brusko et al., 2005; Lindley et al., 2005 ) to no changes when comparing diabetic subjects to healthy control subjects (Putnam et al., 20”
- The PD-1 Pathway in Tolerance and Autoimmunity (2010, background): “Furthermore, effector T cells from T1D individuals may be intrinsically defective.”
- Rapamycin Promotes Expansion of Functional CD4+CD25+FOXP3+ Regulatory T Cells of Both Healthy Subjects and Type 1 Diabetic Patients1 (2006, background): “(22) that CD4 CD25 T cells are reduced in T1D subjects, it is now ascertained that the frequency of CD4 CD25 /bright T cells in T1D patients is similar to that of healthy controls (12, 13, 23).”