ABSTRACT
The discovery of functionally diverse type 1 and type 2 CD4+ T helper cells has provided a cellular basis to explain the development of polarized versions of the immune response (1-3). An abundance of data now strongly suggests that inflammatory immune responses or DTH reactions are primarily mediated by T helper 1 (Th1) populations that are characterized by secretion of interferon (IFN)-γ and tumor necrosis factor (TNF), but little interleukin (IL)-4. By contrast, Th2 cells produce IL-4, IL-5 and IL-13, and mediate immune responses characterized by high levels of non-complement binding IgG, IgE and eosinophil-mediated cytotoxicity, but no organspecific tissue destruction. Th2 cells may also exert an anti-inflammatory action by negatively regulating Th1 cell-mediated immune responses. Although individual cells may exhibit a more complex and heterogeneous pattern of cytokine production, many experimentally induced and naturally occurring autoimmune responses show patterns of cytokine production and effector reactions that are clearly indicative of Th1 responses. Thus, although the diversity of T cell-dependent immunity cannot be fit easily into the Th1/Th2 paradigm, understanding the factors that influence the generation and the effector function of Th1 and Th2 cells is important for the development of therapeutic approaches to fighting a variety of human diseases. This chapter focuses on the inflammatory role of Th1 cells and on the role of cytokines in regulating Th1 differentiation and effector function.
