response on subsequent encounters with a pathogen (Seder and Hill, 2000; Sprent and Surh, 2001).

Cumulative studies have shown αβ-T- and B-lymphocytes are the primary mediators of immunity. Their function is under the control of dendritic cells (DC), the sentinel antigen presenting cells (APC) in peripheral lymphoid tissue that capture and process pathogen derived antigens for presentation to CD4+ and CD8+ subsets of αβ-T-lymphocytes (Banchereau and Steiman, 1998; Flores-Romo, 2001; Huang et al., 2000; Iwasaki and Kelsall, 2000; Kelsall and Strober, 1996). Following uptake of antigen at sites of infection, DC migrate to secondary lymphoid organs, where they present signatory peptide fragments of antigens to CD4+ and CD8+ T-lymphocytes in association with major histocompatibility complex (MHC) class II or I molecules, respectively. Second signals mediated through co-stimulatory molecules expressed on DC, and secreted chemical messengers (chemokines and cytokines) modulate differentiation and maturation of T-lymphocytes to cells with specific effector and/or memory activity (Banchereau and Steinman, 1998; Dubois et al., 1998; Flores-Romo, 2001; Moser and Murphy, 2000). In particular, secretion of IL-12 by DC promotes differentiation of CD4+ lymphocytes with a type 1 cytokine profile dominated by secretion of IFN-γ (Bloom, 1992; Dubois et al., 1998). Lymphocytes with this cytokine profile develop into effector cells that function in CMI and provide help in activation of B cells that produce complement-fixing antibodies. IFN-γ secreted by type 1 CD4+ lymphocytes activates macrophages and increases their capacity to kill ingested bacteria. Direct killing of bacteria is mediated by secretion of perforin and granulysin at the sites of infection (Canaday et al., 2001; Dieli et al., 2001; Smyth et al., 2001). Down-regulation of secretion of IL-12 promotes differentiation of CD4+ lymphocytes with a type 2 cytokine profile dominated by secretion of IL-4. Lymphocytes with this cytokine profile function as helper cells that stimulate activation of B cells that produce antibodies without complement fixing activity. DC also promote differentiation of CD4+ lymphocytes with a type 3 cytokine profile dominated by expression of IL-10 and TGF-β. Lymphocytes with this cytokine profile modulate the maturation of lymphocytes with type 1 and type 2 cytokine profiles by down regulating their effector activity. Stimulation of CD8+ T-lymphocytes by DC promotes differentiation of cytotoxic T-lymphocytes (CTL) with a type 1 cytokine profile and/or T-lymphocytes with a type 2 cytokine profile that regulate CD4+ and CD8+ T-lymphocyte effector activity. The role of DC in the response of γδ-T-lymphocytes is not clear, but may involve the interaction with another MHC related molecule, CD1 (Spada et al., 2000). A subset of γδ-T-lymphocytes in humans has been shown to be selectively activated through CD1c. This subset contains perforin and granulysin and, when activated, secrete IFN-γ and IL-2 (Spada et al., 2000). Granulysin-dependent killing has also been reported for γδ-T-lymphocytes expressing a specific arrangement of the γδ-T-cell receptor (Dieli et al., 2001).

The magnitude and type of immune response depends on the pathogen and in part on which receptors are used for internalization of the pathogen and which signaling pathways are used for antigen processing (Huang et al., 2001;