The adaptive immune responses are orchestrated by the T cells, and T-cell derived cytokines produced in response to specific antigens are not only responsible for leukocyte generation/expansion, recruitment, activation, and antibody responses, but also for contraction and resolution of inflammation. The first account of T-helper (Th) cell subsets characterized by differential cytokine production and function was reported almost 25 years ago. Mosmann and colleagues defined these clones as type 1 Th (Th1) cells and type 2 Th (Th2) cells, and postulated that these T-cell subsets have distinct functions in the immune responses [1,2]. Subsequently, the immune responses driven by these cells were defined as Th1 and Th2 immune responses. The Th1 response is promoted by interleukin-12 (IL-12), interferon-γ (IFN-γ), and tumor necrosis factor-α (TNF-α). The two latter cytokines are also the major products of Th1 cells [2]. Th1 cells are involved in delayed-type hypersensitivity reactions and cell-mediated immunity, are associated with vigorous proinflammatory responses [3], and induce immunoglobulin G class 2a (IgG2a) antibody production by B cells [4]. The Th2 immune response is characterized by IL-4, IL-5, IL-9, IL-10, and IL-13 production by T cells [2], IgG1 and IgE antibody production by B cells [4], and the presence of eosinophilic inflammation [5–7]. The Th1 and Th2 responses counter-regulate each other predominantly by means of the IL-4–IFN-γ negative feedback loop [8,9]; however, other cytokines can be also involved in Th1–Th2 regulation. Both Th1 and Th2 reactions are important in a variety of immune-regulated conditions such as allergies, autoimmune diseases, transplant rejection versus tolerance, and clearance of infectious pathogens, including fungi.