The diabetic BB rat. Neither Th1 nor Th2?
A long term objective of our work has been to identify and characterize the T cells responsible for causing autoimmune type I diabetes in the spontaneously diabetic BB rat. Based on the Th1/Th2 paradigm encompassing "regulated" and "regulatory" T cells, our analyses show that there are very few "regulatory" peripheral Th2 cells. The "regulated" T cells that remain express an unusual, immature phenotype that is neither Th1 nor Th2. Our data also indicate that transcript expression for p56lck, an enzyme required for T cell development, is abnormal in BB peripheral T cells. We discuss the role abnormal transcript expression of p56lck might play in retarding the development of mature regulatory Th2 cells while simultaneously influencing the escape of autoreactive T cells from the thymus.
Bellgrau
D
D
Barbara Davis Center for Childhood Diabetes, University of Colorado Health Sciences Center, Denver, USA.
Stenger
D
D
Richards
C
C
Bao
F
F
D000818:Animals; D003922:Diabetes Mellitus, Type 1 / Q000276:immunology*; D019860:Lymphocyte Specific Protein Tyrosine Kinase p56(lck); D051381:Rats; D011913:Rats, Inbred BB; D018417:Th1 Cells / Q000502:physiology*; D018418:Th2 Cells / Q000502:physiology*; D019061:src-Family Kinases / Q000502:physiology
D019860:Lymphocyte Specific Protein Tyrosine Kinase p56(lck); D019061:src-Family Kinases