Table 5-12. IMMUNE RESPONSE TO FOREIGN/ALTERED-SELF GRAFT

Innate Response


Infiltration of tissue site by phagocytes, natural killer cells and suppressor/cytotoxic T-cells
Antigen-MHC class I glycoprotein recognition
Tissue destruction by cytotoxins (eg., perforin)


Primary Adaptive Response


Phagocytosis of antigen by macrophages and other cells of the reticuloendothelial system
Antigen-presenting cells (APCs) display degraded fragments of antigen bound to an MHC class II glycoprotein
Helper T-cells bind to APCs (the T-cell receptor recognizes the antigen-MHC II complex)
IL-1 secreted by activated APCs induces IL-2 secretion and receptor synthesis by helper T-cells
Helper T-cells proliferate (clonal expansion) in an autocrine fashion due to growth-promoting properties of IL-2
B-lymphocytes also bind and process antigen (virgin cells carry antibodies on their cell surface)
Helper T-cells bind to B-cells
B-cells synthesize receptors for IL-4/helper T-cells secrete IL-4 (B-cell growth factor)
Activated B-cells divide
IL-4 stimulates B-cell synthesis of IL-5 receptors/helper T-cells produce IL-5 (B-cell differentiation factor)
B-cells differentiate into plasma cells and memory cells
Short-lived plasma cells secrete antibodies (IgM then IgG)
Long-lived memory (primed) cells retain cell surface antibodies as antigen receptor
Cell killing by antibody-dependent cell- and(or) complement-mediated mechanisms
Opsonized cells are phagocytosed


Secondary Adaptive Response


Reaction to challenge is similar to above but much faster and more potent (primed memory cells are present)
Memory B-cells divide and some differentiate into plasma cells
Hypersensitivity reactions