THE DIABETIC BB RAT NEITHER TH1 NOR TH2

A long term objective of our work has been to identify and characteriz e the T cells responsible for causing autoimmune type I diabetes in th e spontaneously diabetic BB rat. Based on the Th1/Th2 paradigm encompa ssing ''regulated'' and ''regulatory'' T cells, our analyses show that there are very few ''regulatory'' peripheral Th2 cells. The ''regulat ed'' T cells that remain express an unusual, immature phenotype that i s neither Th1 nor Th2. Our data also indicate that transcript expressi on for p56lck, an enzyme required for T cell development, is abnormal in BB peripheral T cells. We discuss the role abnormal transcript expr ession of p56lck might play in retarding the development of mature reg ulatory Th2 cells while simultaneously influencing the escape of autor eactive T cells from the thymus.