Cytokines are critical mediators in autoimmunity and a better understanding of their mode of action should contribute to the development of strategies for controlling harmful autoimmune reactions. Their complicated nature makes it difficult to classify them as pro- or anti-inflammatory mediators; redundancy in their mode of action has been widely reported. Their complexity is further exemplified by the fact that several cytokines display redundancy in their receptor usage, with the recently identified IL-12 and IL-10 families being prototypical examples. Several aspects--including kinetics of expression, mode of induction, regulation of receptor expression and competition for occupancy, and the stage (acute vs chronic) of the disease--are critical to the net effect, and all these aspects need to be understood if we are to define a cytokine's whole nature.