The fundamental basis of immunity to infectious diseases involves a complex interplay between humoral and cell-mediated immune responses against antigens on the foreign pathogen. Humoral immunity, either in the form of local IgA antibodies at the mucosal site of infection or neutralizing antibodies in the serum, provides the first line of defense against invading microorganisms. However, cellular immunity, mediated by T-cells, also plays a major role in protection against foreign pathogens. CD80+ cytotoxic T-lymphocytes (CTL) kill target cells infected with viruses or bacteria, whereas CD4+ T helper (Th) cells provide help for B-cells in antibody production and secrete a range of cytokines that are involved in a variety of immunoregulatory functions or have a direct effect on invading microorganisms (1 –3 ). The CD4+ T-cell population can further be divided into two subpopulations on the basis of their function and cytokine secretion (4 ). Thl cells secrete interleukin 2 (IL-2), γ-interferon (IFN-γ), and tumor necrosis factor-β (TNF-β) and are involved in delayed-type hypersensitivity and inflammatory responses, and display CTL activity in vitro. A key function of this CD4+ Thl population in the immunological defense mechanism in vivo appears to be the activation of macrophages, which are stimulated to take up and kill invading microorganisms.