The following points highlight the eight main types of interaction between antigen and antibody. The types are: 1. Neutralization 2. Immune Complex Formation 3. Opsonization 4. Complement System 5. Antibody-Dependent Cell-Medicated Cytotoxicity (ADCC) 6. Hypersensitivity 7. Autoimmunity 8. Immuno-Deficiencies.
Certain antibodies called neutralizing antibodies react with antigen and neutralize them so that they fail to attach on host cell surface.
i. Toxin Neutralization:
Toxin neutralization (Fig. 41.15) is the process during which antibodies capable neutralizing a toxin (neutralizing antibodies) or antiserum containing neutralizing antibodies against a toxin inactivate the toxins produced by bacterial pathogens. These neutralizing antibodies or antiserum containing neutralizing antibodies are called antitoxins.
Once neutralized, the toxin-antibody complex is either unable to attach to receptor sites on host target cells, unable to enter the cell, or it is ingested by macrophages. However, bacterial pathogens causing tetanus, diphtheria, etc. are some toxin-producing bacteria.
ii. Viral Neutralization:
Viral neutralization is the process during which specific antibodies (IgG, IgM, and IgA) bind to viruses and inactivate them (Fig. 41.16). Viral neutralization prevents viral infection due to the inability of virus to bind to and enter its target cell. However, fixation of the classical pathway, especially the complement component C3b to the virus, also aids to viral neutralization process.
2. Immune Complex Formation:
Antibodies possess at least two antigen-binding sites and most antigens have at least two epitopes (antigenic determinants). The antibodies cross-link antigens forming large aggregates of antibody and antigen referred to as immune complexes (Fig. 41.17), which are more readily phagocytized than are free antigens.
Depending upon their physical properties, immune complex forming antibodies are of two types: precipitins and agglutins. The precipitins react with antigens that are soluble molecules and form immune complex large enough to precipitate: this process is called precipitation (L. praecipitare = to cast down) or precipitin reaction.
The agglutins, however, react with surface-bound antigens of bacterial or other cells and form immune complex. This process is called agglutination or agglutin reaction. Agglutination specifically involving red blood cells is called hem-agglutination and is caused by antibodies called hemagglutin.
Opsonization (G. opson = to prepare victim for) or opsonin-dependent recognition is one of the two fundamental molecular mechanisms used by phagocytic cells for the recognition of microbial pathogens and their adherence on phagocyte’s plasma membrane so that the phagocytes can ingest them easily.
4. Complement System:
Complement fixation refers to the ability of antigen-antibody-complex to bind complement so that the latter becomes “fixed” and “used up”. It is operated by a system called the complement system which consists of over 30 soluble and cell-bound proteins and glycoproteins that interact in a highly regulated cascade. This system involves in antigen-antibody interaction in host to play its role in immune response.
5. Antibody-Dependent Cell-Medicated Cytotoxicity (ADCC):
Many cells that have cytotoxic potential express membrane receptors for the Fc region of the antibody molecule. When antibody is specifically bound to a target cell, the receptors of these cells can bind to the antibody Fc region. Thus the cytotoxic cells bind to the target cells, and subsequently cause lysis of the target cells.
Although these cytotoxic cells are nonspecific for the antigen, the specificity of the antibody bound to the target cells directs the cytotoxic cells to specific target cells. This type of cytotoxicity is referred to as antibody- dependent cell-mediated cytotoxicity (ADCC).
The cells that can mediate ADCC are NK cells, macrophages, monocytes, neutrophils, and eosinophils. ADCC to cells infected with the measles virus can be observed in vitro by adding anti-measles antibody together with macrophages to a culture of measles-infected cells. Similarly cell-mediated killing of helminths, such as blood flukes, can be observed in vitro by incubating larvae with antibody specific to the larvae together with eosinophils.
ADCC appears to involve a number of different cytotoxic mechanisms, but it does not involve complement-mediated lysis (Fig. 41.18, Table 41.8) When macrophages, neutrophils or eosinophils bind to a target cell, they become more active metabolically. As a result, thelytic enzymes in their cytoplasmic lysosomes (often referred to as granules) increase in quantity.
Release of these lytic enzymes at the site of the Fc-mediated contact may result in damage to the target cell. In addition, activated monocytes, macrophages, and NK cells have been shown to secrete tumor necrosis factor (TNF), which may have a cytotoxic effect on the bound target cell. Since both NK cells and eosinophils contain perform in their cytoplasmic granules, their target-cell killing also may involve perforin-mediated membrane damage.
Hypersensitivity is a condition of increased immune sensitivity in which the body reacts to an antigen with an exaggerated immune response that usually harms the individual by tissue damage. Hypersensitivity, also termed an allergy, is manifested in the individual on second or subsequent contact with an antigen and appears immediate or delayed.
Autoimmunity is a condition characterized by the presence of serum, autoantibodies and self-reactive lymphocytes (T-cells).
Autoimmunity (also the autoimmune diseases) manifests sometimes when the body loses immune tolerance (body’s condition to distinguish its own self-antigens from foreign non-self-antigens and not mounting an immunogenic attack against the former) and mounts an abnormal immune attack, either with antibodies or T-cells, against a person’s own self-antigens.
Immunodeficiency refers to the inability of the immune system to produce a normal complement of antibodies or immunologically sensitive T-lymphocytes in response to self-antigens. Such inabilities of the immune system can make the host more prone to infection and, as a result, the host may become unable to protect itself from disease causing agents or from malignant cells.