explain what is meant by an antigen (see 4.1.3) and state the difference between self antigens and non-self antigens

Immune System – Antigens and Immune Responses (Topic 11)

1. Definition of Antigen (11.1 1)

Antigen: “any substance that can be recognised by the immune system and that elicits an immune response.”

In the Cambridge syllabus antigens are usually proteins or polysaccharides located on the surface of:

• the body’s own cells,
• viruses and bacteria,
• toxins,
• transplanted tissue, or
• allergens.

2. Self‑Antigens vs. Non‑Self Antigens (11.1 2)

3. Phagocytes – Mode of Action (11.1 3)

• Ingestion (phagocytosis): Neutrophils and macrophages surround and engulf particles > 0.5 µm.
• Destruction: Lysosomal enzymes and the oxidative burst (reactive oxygen species) kill the ingested micro‑organism.
• Antigen presentation: Processed peptide fragments are displayed on MHC II molecules of the macrophage for recognition by CD4⁺ T‑helper cells.

Diagram suggestion: labelled macrophage showing engulfed particle, lysosome, oxidative burst, and MHC II‑peptide complex.

4. Primary Immune Response – Sequence of Events (11.1 4)

1. Antigen capture – Macrophage engulfs the pathogen and presents antigen on MHC II.
2. Activation of T‑helper (Th) cells – Th‑cell receptors bind the antigen‑MHC II complex; cytokines are released.
3. Activation of B‑cells – B‑cell receptors bind the same antigen; cytokine help from Th cells drives B‑cell proliferation.
4. Plasma‑cell formation – Differentiated B‑cells become plasma cells that first secrete IgM antibodies.
5. Class switching (IgM → IgG) – Later in the primary response, cytokines induce switching to IgG, which has higher affinity.
6. Effector phase – Antibodies neutralise the pathogen, opsonise for phagocytosis, or activate complement.

5. Secondary Immune Response – Memory (11.1 5)

• During the primary response a proportion of activated B‑cells and T‑cells become long‑lived memory B‑cells and memory T‑cells.
• On re‑exposure to the same antigen the secondary response is characterised by:

  • faster onset,
  • larger quantity of antibody,
  • predominant production of high‑affinity IgG.

• This rapid, vigorous response underlies the principle of vaccination.

6. Antibodies – Structure ↔ Function (11.1 6)

• Y‑shaped glycoproteins composed of two identical heavy chains and two identical light chains.
• The tips of the “Y” form the antigen‑binding (Fab) region; each antibody can bind two identical epitopes.
• The stem (Fc region) determines the antibody class and mediates effector functions such as complement activation or binding to phagocyte receptors.

7. Vaccination – Active vs. Passive Immunity (11.1 7)

• Active immunity: Exposure to a harmless form of antigen stimulates the body’s own immune system to produce memory cells and antibodies.

  • Example: live‑attenuated measles‑mumps‑rubella (MMR) vaccine.

• Passive immunity: Pre‑formed antibodies are transferred to an individual; protection is immediate but short‑lived because no memory cells are generated.

  • Example: maternal IgG transferred across the placenta; antiserum given after rabies exposure.

8. Hybridoma Technology – Production of Monoclonal Antibodies (A‑Level only)

Step‑wise outline required by the syllabus:

1. Immunise a mouse with the desired antigen.
2. Harvest spleen B‑cells that produce the specific antibody.
3. Fuse the B‑cells with an immortal myeloma cell line to create hybrid cells (hybridomas).
4. Select hybridomas in HAT medium; only fused cells survive.
5. Screen hybridoma supernatants for the desired antibody specificity.
6. Clone the positive hybridoma to obtain a line that secretes identical (monoclonal) antibodies indefinitely.

Monoclonal antibodies are used in diagnostics, targeted cancer therapy, and research.

9. MHC & Antigen Presentation (implicit in primary response)

• MHC I presents endogenous (intracellular) peptide fragments to CD8⁺ cytotoxic T‑cells.
• MHC II presents exogenous (extracellular) peptide fragments to CD4⁺ T‑helper cells – the crucial link between phagocytosis and the adaptive response.

Key Points to Remember

1. Antigen = any substance recognised by the immune system that elicits a response.
2. Self‑antigens are tolerated (immune tolerance established during development); non‑self antigens provoke immunity.
3. Phagocytes ingest, destroy (lysosomal enzymes + oxidative burst), and present antigens on MHC II.
4. Primary response sequence: (i) antigen capture → (ii) Th‑cell activation → (iii) B‑cell activation → (iv) plasma‑cell formation (IgM → IgG class switching) → (v) effector phase.
5. Memory B‑cells and T‑cells give a faster, larger IgG‑dominant secondary response.
6. Antibody structure (Y‑shape) explains Fab (binding) and Fc (effector) functions; five isotypes have distinct roles.
7. Active immunity (e.g., live‑attenuated vaccine) creates memory; passive immunity (e.g., maternal IgG) provides temporary protection.
8. Failure of self‑tolerance leads to autoimmunity; foreign antigens cause infection, transplant rejection, allergy, or vaccine‑induced protection.