There are more than 1,000,000 different types of antibodies performing surveillance for invading foreign antigens that enter the body.
Antibodies are Y-shaped proteins with two arms that act as antigen-binding sites (Fab), and a base (Fc) that determines the class of antibody. Antibodies are also referred to as gamma-globulins or immunoglobulins, and are named according to their functions – agglutinins, precipitins, hemolysins, etc.
The base of the Y is made of heavy chains, while its arms are made of both light and heavy chains. The tips of the arms contain a cavity with a shape unique for the shape of the protein fragment (antigen) that the antibody is specific for.
There are five general classes of immunoglobulins:
- IgG
- IgA
- IgM
- IgE
- IgD
IgG
- account for 75% of plasma antibody
- produced in secondary immune response
- cross the placental membrane
IgA
- found in secretions such as saliva, tears, intestinal and bronchial mucus, as well as breast milk
- disable invaders
IgE
- allergic responses
- IgE/antigen complex stimulates mast cells to release histamine
IgM
- activates complement
- reacts to blood group antigens
IgD
- found on surface of B-lymphocytes
- role unclear
Immune Response to Bacterial infection
When body surface barriers fail and bacteria reach the extracellular fluid, an inflammatory response develops as immune cells defend the body against further penetration and invasion. A series of events occurs:
- Phagocytes and NK-cells migrate to the area in response to cytokines sent by emergency responders at site of invasion, and ingest and/or destroy bacteria.
- TC-cells appear as T-cells are activated by antigen presentation.
- Plasma cell production increases as activated B-cells differentiate.
- Surge in plasma cell production is followed by gradual decrease and sustained levels of circulating antibodies.
The complement system is activated by components of the bacterial cell wall:
- Complement causes degranulation of mast cells and basophils.
- Cytokine release attracts more immune cells, dilates blood vessels and increases capillary permeability.
- Increased blood flow to the area results in inflammation, and plasma proteins and water passing into the interstitial spaces results in edema.
- Membrane attack complex (MAC) molecules blow holes in the bacterial cell wall resulting in plasma influx resulting in lysis and death (e.g. navy divers plant charges on hull of ship to sink the ship) .
- Macrophages ingest bacteria.
- Opsonization of encapsulated bacteria .
- Acquired immune response – antibodies already present act as opsonins and also inactivate bacterial toxins.
- Memory B-cells attracted to infection site activated by antigens that they recognize (similar to a police line-up).
If blood vessels are also damaged, platelets and coagulation proteins help reduce damage
The initial steps in response to viral invasion are different from those involved in bacterial invasion. Phagocytes digest and disassemble viruses and display viral antigen fragments on MHC proteins on the cell surface activating TC-cells and NK-cells. In addition to activation by antigen presenting phagocytes (APC), TC-cells and NK-cells are activated by contact with antigen-presenting phagocytes or virus-infected tissue cells.
Viruses bind to cell membranes in the body and cross the cell membrane by binding to membrane receptors and triggering endocytosis, a process similar to phagocytosis, except that the cell membrane indents rather than pushing out around the particle to be ingested. Alternatively, the viral envelope fuses with the cell membrane, injecting the virus core into the cytoplasm.
Once inside the cell, the virus uses the cell’s resources to replicate, creating new viral nucleic acid and viral proteins, which assemble to new virus particles, are released from the cell, and subsequently infect new cells. In the process, host cell function may be disrupted resulting in cell death, or may be temporarily disrupted by viruses which reproduce only sporadically (e.g. Herpes simplex type 1). Other viruses (e.g. HIV) incorporate viral DNA into host cell DNA and reproduce.
Viruses are released through cell rupture or they cloak themselves in a capsule of host membrane and escape through the cell surface unnoticed.
Innate immune response and antibodies are involved in defense against acute viral infection. However, once viral particles enter host cells, TC-cells form the main line of defence, searching for infected host cells and destroying them, much like hit-men deployed to locate and eliminate traitors)
Antibodies play an important role in acute viral infection:
- act as opsonins and coat the viral particle to enhance their visibility to macrophages
- bind to virus to prevent entry into cells
- macrophages ingest viruses and insert fragments in cell membrane bound to MHC molecules and produce cytokines – cytokines initiate the inflammatory response; one of these, interferon, causes host cells to make antiviral proteins that prevent viral replication
- TH-cells bind to viral antigen fragments on macrophages and enhance immune cell response
- TC-cells recognize viral antigen fragments bound to MHC complexes and induce the cell to commit suicide (apoptosis).
