The
nuclear factor-kappaB (
NF-kappaB) family of
transcription factors is activated by many infectious and inflammatory stimuli. This family regulates the expression of multiple genes, whose products include
cytokines,
chemokines, adhesion molecules, and antiapoptotic factors that are important components of the innate and adaptive immune response. A prominent role of
NF-kappaB transcription factors in resistance to a variety of
infectious diseases was revealed by studies with mice that lack individual family members. However, little is known about the basis for these effects or about the role of individual family members during a coordinated immune response to
infection. Diverse parasites such as Toxoplasma gondii, Leishmania major, and Trichuris muris provide a unique opportunity to understand the role of the
NF-kappaB system in the development of innate and adaptive immunity to these
infections. The basis for resistance and susceptibility to these parasites is well understood, and studies using these experimental systems have provided unique insights into the role of
NF-kappaB in the regulation of T-helper 1 cell (Th1) and Th2 type responses. It has become clear that
NF-kappaB family members have cell lineage-specific functions and that their relative importance varies with type of
infection as well as route of pathogen entry. Thus, studies with models of
parasitic infection have revealed that individual
NF-kappaB family members perform distinct, nonoverlapping, and biologically significant functions in the regulation of immunity and
inflammation.