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Novel leptin receptor mutation in NOD/LtJ mice suppresses type 1 diabetes progression: II. Immunologic analysis.
Partial versus full allogeneic hemopoietic chimerization is a preferential means to inhibit type 1 diabetes as the latter induces generalized immunosuppression.
Enhanced responsiveness to T-cell help causes loss of B-lymphocyte tolerance to a ?-cell neo-self-antigen in type 1 diabetes prone NOD mice.
Subcongenic analyses reveal complex interactions between distal chromosome 4 genes controlling diabetogenic B cells and CD4 T cells in nonobese diabetic mice.
Cellular expression requirements for inhibition of type 1 diabetes by a dominantly protective major histocompatibility complex haplotype.
The CD137 Ligand Is Important for Type 1 Diabetes Development but Dispensable for the Homeostasis of Disease-Suppressive CD137+ FOXP3+ Regulatory CD4 T Cells.