By virtue of their functional antagonism, Th1 cells or cells producing
the same cytokines as Th1 cells may behave as 'suppressor cells' with
respect to Th2 cells and vice versa, An excessive Th1- or Th2-like re
sponse may favor the development of different autoimmune diseases, As
can be expected from their physiological role, Th-l cytokines particip
ate in autoimmune diseases with a preferential delayed type hypersensi
tivity component, i.e. in those diseases in which cytotoxic T cells at
tack organ-specific target cells, Autoimmune diseases with a predomina
nt Th1 component include experimental autoimmune encephalitis and insu
lin-dependent diabetes mellitus, In contrast, Th2-type responses parti
cipate in systemic autoimmune diseases with a strong humoral component
, Such diseases probably include certain drug-induced states of autoag
gression, namely mercury-induced autoimmune disease and chlorpromazine
-induced autoimmunity, It is tempting to speculate that therapeutic in
terventions designed to recover a normal Th1/Th2 balance will provide
a useful etiological strategy for the re-establishment of self-toleran
ce.