01 · Innate immunity
The first lines of defence
Innate immunity is the body's immediate, non-specific response to pathogens. It has three layers:
01
Physical barriers
Skin (keratinised epithelium), mucus membranes (trap pathogens), cilia (sweep debris up the respiratory tract), stomach acid (pH ~2 kills most bacteria), lysozyme in tears and saliva.
02
Cellular response
Pattern recognition receptors (TLRs, NODs) on innate cells recognise conserved pathogen-associated molecular patterns (PAMPs). Neutrophils and macrophages engulf and destroy invaders. Natural killer cells kill infected host cells.
03
Complement and inflammation
The complement cascade (>30 proteins) marks pathogens for destruction (opsonisation), lyses bacterial membranes, and recruits immune cells. Cytokines (IL-1, IL-6, TNF-α) produce fever and recruit more immune cells to the site.
The inflammatory response — redness, heat, swelling, pain — is not a failure of immunity but a feature: vasodilation increases blood flow and vascular permeability, delivering immune cells and proteins to the infection site. See Homeostasis for how fever is regulated and when it becomes dangerous.
02 · Adaptive immunity
Specific, memorable, and devastating
When innate defences are overwhelmed (or in parallel), the adaptive immune system generates a pathogen-specific response. It takes 4–7 days for a primary response but creates immunological memory — re-exposure triggers a faster, stronger secondary response within hours.
The cellular cast
| Cell type | Arm | Key role |
|---|---|---|
| Neutrophil | Innate | First responder phagocyte; engulfs and destroys bacteria |
| Macrophage | Innate | Phagocytosis; antigen presentation; secretes cytokines |
| Dendritic cell | Innate→Adaptive | Professional antigen-presenting cell; activates naïve T cells |
| Natural killer cell | Innate | Kills virally infected and tumour cells without prior sensitisation |
| B cell | Adaptive | Produces antibodies; differentiates into plasma cells and memory B cells |
| CD4⁺ T helper | Adaptive | Activates B cells, CD8⁺ T cells, and macrophages; coordinates immune response |
| CD8⁺ cytotoxic T | Adaptive | Kills infected cells and cancer cells displaying foreign antigen on MHC I |
| Regulatory T cell | Adaptive | Suppresses immune response; maintains self-tolerance; prevents autoimmunity |
Clonal selection and affinity maturation
Each naïve B and T cell has a unique antigen receptor generated by V(D)J recombination — a DNA rearrangement that creates ~10¹² different receptor specificities. On encountering its specific antigen (presented on MHC molecules by dendritic cells), a T cell or B cell proliferates clonally. B cells in germinal centres undergo somatic hypermutation, and cells with higher-affinity antibodies are selected — affinity maturation.
This connects deeply to genetics and inheritance: V(D)J recombination is somatic DNA rearrangement (not inherited), and somatic hypermutation is directed mutation in the antibody gene. The immune system effectively evolves antibodies within a single organism's lifetime.
03 · Vaccines
How vaccines exploit immunological memory
A vaccine presents antigen to the adaptive immune system without causing disease. The immune response generates memory B and T cells. On later exposure to the real pathogen, these memory cells enable a secondary response that is:
- Faster — hours instead of days
- Stronger — higher antibody titres, more T cells
- Higher affinity — somatic hypermutation has already optimised the antibodies
Vaccine types include: live attenuated (measles, MMR), inactivated (flu shot, polio Salk), subunit (hepatitis B, HPV), toxoid (tetanus, diphtheria), viral vector (Oxford-AZ COVID-19), and mRNA (Pfizer/BioNTech, Moderna COVID-19). For the molecular mechanism of mRNA vaccines — how ribosomes translate a lipid-nanoparticle-delivered mRNA into the target antigen — see the mRNA vaccines article and the Protein synthesis guide.
The Immune System — common questions
- Innate immunity is fast, non-specific, and does not create memory. Adaptive immunity is slow (4–7 days for primary response), antigen-specific, and generates memory B and T cells that enable a faster secondary response. Both systems communicate: dendritic cells (innate) present antigen fragments on MHC molecules to activate T cells (adaptive).
- Vaccines prime adaptive immunity. mRNA vaccines encode the antigen (e.g. spike protein) directly — ribosomes translate the mRNA into protein, which is presented to T cells and stimulates antibody production. See the mRNA vaccines article for the molecular detail.
- Antibodies are Y-shaped glycoproteins. The variable region (Fab) binds a specific antigen epitope; the constant region (Fc) recruits complement, triggers phagocytosis, or activates NK cells. Affinity maturation in germinal centres selects B cell clones with higher-affinity antibodies. See protein synthesis for how antibody genes are transcribed and translated.
- Central tolerance: self-reactive T cells are deleted in the thymus (negative selection). Peripheral tolerance: regulatory T cells (Tregs) suppress escaping self-reactive cells. Failure of either mechanism leads to autoimmunity. Genetic factors (HLA alleles — see allele) and environmental triggers (infection, gut microbiome — see gut microbiome) both contribute.