External defence system:
- Hydrochloric acid in stomach
- Blood clotting
- Epithelia covering airways act as a barrier
Internal defence system:
- White blood cells recognise pathogens by “large molecules on surfaces” such as proteins, glycolipids, glycoproteins etc.
- Antibodies (glycoprotein molecules) are produced against non-self-antigens.
Immune system cells:
Phagocytes and Lymphocytes.
- Neutrophils: 60% of white blood cells. Short lived cells which leave the blood by squeezing through capillaries. Engulf pathogens they find. Released in large numbers during an infection.
- Macrophages: Larger than neutrophils. Travel in blood as monocytes and settle in organs. Found in organs such as lungs, liver, spleen, kidney, lymph nodes. Long lived cells which cut up pathogens to display antigens.
- Cells under attack release histamine
- Neutrophils are attracted (chemotaxis).
- Neutrophils have receptor proteins on their surface that recognise antibody molecules on the pathogen and attach to them.
- Neutrophil’s cell surface membrane traps pathogens within a phagocytic vacuole in a process – endocytosis.
- Lysosomes fuse with phagocytic vacuole and break down the pathogen.
Dead neutrophils collect and form pus.
- Immature B cells divide by mitosis in bone marrow.
- Receptors are produced using antibody molecules.
- Receptors on cell surface membrane recognise antigens.
- B cells with receptors complementary to antigen are stimulated to divide by mitosis, this is clonal selection.
- These “clones” of B lymphocytes then divide by mitosis repeatedly in the “clonal expansion” stage.
- Some B cells become plasma cells and secrete antibodies which some become memory cells which circulate in the body for a long time.
Primary immune response is slower because there are less B cells specific to the antigen.
Secondary immune response is faster as there are many memory cells which can divide rapidly to differentiate into plasma cells.
Antibodies: Consists of two heavy and two light polypeptide chains held together with disulphide bonds. Antigen binding site forms the “variable” region which varies from one antibody to another.
Function of antibodies:
- Combining with viruses preventing them from entering or damaging cells.
- “Punch” holes in cell walls causes osmotic imbalance and leading to “lysis” (bursting).
- Coat bacteria, making it easier for phagocytes to ingest them. Phagocytes have receptors.
- Attach to flagella, making them less active.
- Can cause agglutination of bacteria if antibodies have multiple binding sites.
- Combine with toxins and neutralise them. (antitoxins)
Recognise cells presented by macrophages.
T- Helper cells:
- Secretes cytokines when activated.
- Cytokines stimulate macrophages to carry out phagocytosis more vigorously.
- Attach to cells and release toxic substances, kill cancer and infected cells.
- Recognise antigens and attach to cells.
Memory T-killer and T-helper cells are produced.
Types of immunity:
- Active immunity: Immunity gained when an antigen enters the body. Antibodies produced.
- Artificial: Antigens put into the body, by mouth or injection.
- Natural: Gained by being infected by a pathogen.
- Passive immunity: Temporary immunity, no immune response.
- Artificial: Gained by injecting antibodies.
- Gained by foetus when maternal antibodies cross the placenta or the immunity gained by an infant from breast milk.
- Preparation containing antigens to stimulate immune response artificially.
- May contain live microorganism, dead one, harmless (attenuated), toxoid.
- Booster injections are needed for less effective vaccines.
Herd Immunity: Vaccinating a large proportion of the population. Transmission of pathogen is reduced and so people who are not immunised are protected.
Monoclonal Antibodies (Mabs): Antibody made by a single clone of hybridoma cells. All antibodies have identical variable regions specific to one antigen.
- Plasma cells producing a particular antibody are fused with cancer cells. Fusion is known as hybridoma.
Mabs are used in treatments for:
- Breast cancer
- Melanoma (skin cancer)
- Rheumatoid arthritis
Note: All images and some texts have been adapted from Cambridges AS and A level Biology Coursebook.