The Adaptive Immune System
High-Yield Summary
- Humoral immunity (B cells, antibodies) targets extracellular pathogens; cell-mediated immunity (T cells) targets intracellular pathogens and abnormal cells directly.
- Antibodies: variable region (antigen-binding, unique per antibody) + constant region (same within a class). Fight pathogens via neutralization, opsonization, agglutination, degranulation.
- Clonal selection explains why the secondary immune response (memory B cells already standing by) is faster/stronger than the primary response — the basis of vaccination.
- 4 T cell subtypes: helper (CD4+, via MHC II, coordinate), cytotoxic (CD8+, via MHC I, kill via perforin/granzymes), regulatory (self-tolerance), memory (fast secondary response). HIV destroys CD4+ T cells, crippling coordination.
- Bacterial infections mainly activate the MHC II / CD4+ / B cell / antibody pathway; viral infections mainly activate the MHC I / CD8+ cytotoxic pathway (NK cells back up MHC-I-evading cells).
- Active immunity (exposure/vaccination) = slow but long-lasting via memory cells. Passive immunity (transferred antibodies) = immediate but temporary.
Key Terms
- Clonal selection
- Only B/T cells with receptors specific to the antigen proliferate, forming an army of identical cells.
- Isotype switching
- B cells changing antibody class (IgM/IgD/IgG/IgE/IgA) in response to cytokines — changes function, not antigen specificity.
- Perforin & granzymes
- Released by cytotoxic T cells: perforin pokes pores in the target membrane, granzymes trigger apoptosis.
- Self-tolerance
- Immune cells reactive to self-antigens are eliminated during development, preventing autoimmune attack.
- Hypersensitivity reaction
- Exaggerated immune response to a harmless foreign substance (e.g., allergies).
Primary vs. Secondary Immune Response
| Primary Response | Secondary Response |
|---|---|
| First antigen encounter | Repeat antigen encounter |
| Slow — naïve B cells must activate and expand | Fast and strong — memory B cells already standing by |
| No pre-existing memory cells | Basis of vaccination |
T Cell Subtypes
- Helper T cells (CD4+)
- Recognize antigens on MHC II; secrete signals that activate B cells, cytotoxic T cells, and macrophages.
- Cytotoxic T cells (CD8+)
- Recognize antigens on MHC I; kill via perforin + granzymes. Target virus-infected/cancer cells.
- Regulatory T cells
- Maintain self-tolerance; prevent immune overactivation and autoimmune disease.
- Memory T cells
- Long-lived cells enabling a rapid, strong response if the same pathogen returns.
Common MCAT Trap
- Isotype switching changes antibody FUNCTION (isotype: IgM→IgG etc.), NOT the antigen specificity — don't confuse it with affinity maturation.
- HIV targets CD4+ helper T cells specifically, not cytotoxic T cells directly — the damage is to immune coordination, since helper T cells activate B cells, cytotoxic T cells, and macrophages.
- Passive immunity gives NO memory cells (temporary protection) — active immunity does (long-lasting). Maternal antibody transfer is passive, not active.
Quick Recall
What are the 2 parts of an antibody and their roles?
Why is the secondary immune response faster than the primary?
Which T cell subtype does HIV target, and why does that cripple the immune system?
Active vs. passive immunity — which is faster, which lasts longer?