Suppressor T lymphocyte dysfunction is important in the pathogenesis of autoimmune thyroid disease: a perspective. 
Over the past decade, there was considerable scepticism regarding the existence, nature, and function of suppressor T (Ts) lymphocytes, particularly antigen-specific Ts lymphocytes.  The receptors of putative antigen-specific murine Ts hybrids revealed that most either lacked the T cell receptor beta (TCR beta) chain or had failed to properly rearrange them and thus could not make a functional receptor.  Moreover, studies of the DNA of sequences of the MHC I-J region (considered an important determinant for suppression) fail to show evidence for a unique open reading frame capable of encoding the I-J restriction element.  In addition, no molecular basis for suppression had been characterized.  These criticisms have now been satisfactorily resolved and the pendulum is swinging in favor of participation by antigen-specific Ts lymphocytes in immune tolerance.  Ts lymphocytes have now been cloned and cell lines have been found to be idiotypic-specific.  Indeed, specific Ts lymphocytes in the periphery have been shown to prevent the appearance of autoreactivity.  It is, therefore, legitimate to consider their control as part of the mechanisms of maintaining the integrity of the immune system.  Moreover, all human primary Ts clones and the majority of murine Ts clones have now been shown to rearrange TCR alpha beta.  Ts lymphocytes are induced by antigen via antigen-presenting cells (APCs), and may do so in the context of MHC class II antigens, a concept not previously accepted.  Moreover, there is now considerable evidence that such cells many well be involved in various autoimmune disease states.(ABSTRACT TRUNCATED AT 250 WORDS)