title: The diabetic BB rat. Neither Th1 nor Th2?
abstract: 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.
authors.affiliation: Barbara Davis Center for Childhood Diabetes, University of Colorado Health Sciences Center, Denver, USA.
authors.forename: D
authors.initials: D
authors.lastname: Bellgrau
authors.forename: D
authors.initials: D
authors.lastname: Stenger
authors.forename: C
authors.initials: C
authors.lastname: Richards
authors.forename: F
authors.initials: F
authors.lastname: Bao
mesh_terms: 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
chemical_list: D019860:Lymphocyte Specific Protein Tyrosine Kinase p56(lck); D019061:src-Family Kinases