Barriers, phagocytes, and antibodies
Layers of defence.
Pathogens are disease-causing organisms: bacteria, viruses, fungi, protists, prions.
First line β physical and chemical barriers:
- Skin β keratinised; impenetrable to most microbes.
- Mucus in airways traps inhaled microbes; cilia sweep them up.
- Stomach acid (pH 2) kills most swallowed bacteria.
- Lysozyme in tears and saliva digests bacterial cell walls.
- Acidic skin secretions and competition from normal flora.
Second line β innate immune response. When pathogens breach barriers:
- Phagocytes (e.g. macrophages, neutrophils) engulf pathogens by phagocytosis: pseudopodia surround β vesicle forms β lysosome fuses β enzymes digest.
- Inflammation at injury site: histamine causes vasodilation + increased permeability β more phagocytes arrive.
Third line β adaptive immune response (slower but specific and remembered):
- Antigens are unique molecules on pathogen surfaces.
- B-lymphocytes with matching receptor are activated, multiply (clonal selection), and differentiate into plasma cells (antibody-producing) and memory cells.
- T-helper cells coordinate; cytotoxic T cells kill infected cells.
Antibodies are Y-shaped proteins (immunoglobulins) with two specific antigen-binding sites. They:
- Bind to antigens (neutralisation).
- Mark pathogens for phagocytes (opsonisation).
- Cause pathogens to clump (agglutination).
- Activate complement (membrane attack complex).
After infection, memory B and T cells persist β providing rapid, stronger response on re-exposure (immunological memory).
- Physical/chemical barriers first.
- Phagocytes engulf (innate, non-specific).
- Lymphocytes β antibodies (adaptive, specific).
- Memory cells = lasting immunity.