Effector mechanisms of immunity comprise the following: TCR on T-lymphocyte surface and/or immunoglobulins in solution physically convey the bound Ag to specific cells or enzymes destined to break down Ag into small metabolites. The latter is removed by organism through the excretory system (kidney, gastrointestinal tract).
According to two types of Ag-binding Rc there are two types of effector mechanisms:
• Antibody-dependent, previously called humoral immunity;
• T-lymphocyte-dependent (antibody-independent), its previous name is cellular immunity.
ANTIBODY-DEPENDENT MECHANISMS OF PROTECTION Complement components
Pathogen binding is protective in at least two cases:
1. If a pathogen is a strong poison and AB neutralize toxicity when binding;
2. If a pathogen is infectious (virus, prion, bacterium) an AB binds to it and thus prevents pathogen spreading within an organism. In such cases the protective reaction does not conclude by formation of macromolecular complexes "Ag-AB". The complexes are to be split into small metabolites. For this purpose AB fixes and activates complement components (IgM>IgG3>IgG1). The complexes "Ag-AB-complement components" are transported by erythrocytes carrying Rc for complement components into spleen and liver sinusoids to be phagocytosed and lysed by macrophages.
Fc-receptors
FcR are the membrane molecules specifically binding Fc-fragments of Ig. They could be referred (along with TCR and BCR) to as immune receptors because FcR bearing cell is able to bind Ag (may be by means of AB) and react to it. FcR are present both on lymphocytes and all known leukocytes.
Types and variants of FcR. By isotype of Ig heavy chains which they bind 4 variants of FcR are distinguished: y,e,a, and ц; by affinity for ligand binding 3 types of FcR are distinguished: I, II and III. Type I Rc are able to