MI2.1-3 | Innate & Adaptive Immunity — Structure and Function — Summary & Reflection

REFLECT

Consider the following integrative questions before you proceed to the next module:

1. A child with congenital absence of the thymus (DiGeorge syndrome) would have absent T cells but intact B cells. Which infections would this child be most susceptible to, and why?

1. Why might a patient with agammaglobulinaemia (absent B cells and antibodies) still be able to control a primary herpes simplex virus infection, at least partially?

1. The secondary immune response produces predominantly IgG rather than IgM. What mechanisms in the germinal centre explain this class switch, and what is its clinical significance for vaccination?

Think through each before looking at reference texts.

KEY TAKEAWAYS

Key take-home points from this module:

• The immune system has two arms: innate (fast, non-specific, no memory) and adaptive (slow, specific, memory-forming). Both are essential and interconnected.
• Antigens are recognised via epitopes; haptens need carrier proteins to be immunogenic; polysaccharide antigens are T-independent and fail to generate memory in infants under 2 years.
• Antibodies are Y-shaped glycoproteins with Fab (antigen-binding) and Fc (effector) regions. IgM dominates the primary response; IgG dominates secondary responses and crosses the placenta.
• The complement system has three activation pathways (classical, lectin, alternative) converging at C3, producing opsonins (C3b), anaphylatoxins (C3a, C5a), and the MAC (C5b-9) for bacterial lysis.
• Humoral immunity targets extracellular pathogens via B cells → plasma cells → antibodies; germinal centre reactions produce affinity maturation and class switching.
• Cell-mediated immunity targets intracellular pathogens: CD4+ Th cells (MHC II, orchestrate response) and CD8+ CTLs (MHC I, kill infected cells).
• Th1 responses control intracellular pathogens like TB; Th2 responses drive antibody production and eosinophilia in helminth infections.