Interleukin-4 (IL-4) is a type I cytokine which acts on multiple hemopoietic cells to promote an antibody-mediated response to infection. Dysregulated production or function of IL-4 can exacerbate diseases such as allergy, asthma and rheumatoid arthritis. In order to better understand the biochemical mechanisms by which IL-4 mediates its pleiotropic biological effects, I investigated two distinctive aspects of the intracellular signals activated by IL-4. First, IL-4 is different from most type I cytokines in its inability to activate Ras or Raf-1. IL-4 also fails to support cellular growth. I demonstrated that the signals provided by an active Ras or an inducibly active Raf-1 kinase could synergise with IL-4 to promote cell-cycle progression. Further investigation of the biochemical events associated with the stimulation of long-term growth showed that active Raf-1 not only synergised with IL-4 to stimulate growth, but also to increase levels of c-jun N-terminal kinase (JNK) activity. These observations raise the possibility that Raf-1 may be involved in regulating JNK activity, and that JNK may be involved in mediating certain effects of IL-4. Second, IL-4 and IL-13 are the only cytokines that activate the transcription factor STAT-6. I determined that activation of STAT-6 was required for IL-4- stimulated cell survival. However, I found evidence that this requirement for STAT-6 was indirect, and possibly related to STAT-6-dependent, IL-4-stimulated expression of the IL-4 receptor. I next investigated the hypothesis that STAT-6 was required for IL-4-mediated suppression of tumor necrosis factor α (TNFα) and interleukin-12 (IL-12) production in macrophages. When STAT-6 null macrophages were stimulated with lipopolysaccharide (LPS) and interferon γ (IFNγ), I continued to observe a significant inhibition of TNFα and IL-12 by IL- 4, suggesting that IL-4 activates distinct, STAT-6 independent, inhibitory paths. IFNγ antagonizes many of the effects of IL-4, and I determined that IFNγ may regulate the activity of STAT6 by altering expression of a STAT6 inhibitor, Bcl-6. Further investigation into the roles of JNK, Bcl-6 and novel, non-STAT-6-dependent pathways will be important for the design of strategies to therapeutically modulate the intracellular signals activated by IL-4.