Overview Cell-mediated immunity is the result of cooperation between innate and adaptive immunity to destroy virus infected cells before they can produce more virus damage pathogenic bacteria, fungi, and parasites eliminiate cancerous cells that lack normal cell surface proteins Cells involved in immunity can be divided into primary effector cells such as granulocytes macrophages CD8+ T-cells natural killer (NK) cells secondary support cells such as CD4+ helper T-cells dendritic cells Cell-mediated immunity can result from innate immune response activation of T-cells coordination of cells via cytokines Important Cytokines in Cellular Immunity Cytokines are key coordinators of the cellular immune response by promoting vascular changes near the site of inflammation recruiting of other target cells differentiation of target cells signaling to distant organs Cytokines can be secreted by a variety of cells including activated macrophages helper T-cells killer T-cells Important Cytokines in Cellular Immunity Cytokine Function Secreted by Interleukin-1 Causes fever and acute inflammation Activates endothelial expression of adhesion molecules Macrophages Interleukin-2 Stimulates growth and survival of T-cells and NK cells All T-cells Interleukin-3 Stimulates the growth and differentiation of bone marrow cells All T-cells Interleukin-4 Induces differentiation of helper T-cells into Th2 subtype cells Promotes growth of B-cells and enhances class switching to IgG and IgE Th2 cells Interleukin-5 Promotes growth and differentiation of B cells and eosinophils Promotes class switching to IgA Th2 cells Interleukin-6 Stimulates fever Causes increased production of acute phase proteins by liver Macrophages Interleukin-8 Stimulates chemotaxis by neutrophils to sites of infection Macrophages Interleukin-10 Decreases inflammatory response by inhibiting macrophages and dendritic cells Decreases expression of MHC molecules and Th1 cytokines Regulatory T-cells Interleukin-12 Promotes differentiation of T-cells into Th1 cells Activates killing by NK cells Macrophages Tumor necrosis factor-α Alters vascular endothelium to promote leakage Recruits diverse white blood cells to site of release Induce fever Macrophages Interferon-α/β Activates antiviral defense system of cells Down regulates protein synthesis Upregulates MHC expression for easy recognition of infected cells All cells Interferon-γ Activates macrophages to kill ingested organisms Promotes granuloma formation Increases MHC and antigen presentation by all cells Increases killing by NK cells Th1 cells Effector Mechanisms Macrophage and neutrophil killing depends upon oxygen-dependent mechanisms such as respiratory burst oxygen-independent mechanisms including hydrolytic enzymes that destroy peptides defensins that form holes in bacterial membranes lactoferrin that binds iron and denies it to bacteria lysozyme that cleaves bacterial peptidoglycan walls NK and cytotoxic CD8+ T-cell killing depends upon three mechanisms including exocytosis of cytotoxic granules containing granzymes that are apoptosis activating serine proteases perforin that makes a hole in membranes Fas ligand that directly signals target cells to undergo apoptosis cytokine signaling mainly through TNF pathways that also induce apoptosis Notably NK cells are inhibited by MHC complexes on the surface of cells