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.