Questions: Innate Immune Response

Question 1

How does the innate immune system distinguish pathogens from the body's own cells?

• A. It recognizes unique antigens specific to each individual pathogen strain
• B. It detects pathogen-associated molecular patterns (PAMPs) shared by broad classes of pathogens, via germline-encoded pattern recognition receptors
• C. It relies on memory B and T cells from prior infections
• D. It responds only after the adaptive immune system signals it to activate

Answer: (B)

The innate immune system uses germline-encoded pattern recognition receptors (PRRs) — such as Toll-like receptors — to detect conserved molecular structures (PAMPs) found on bacteria, viruses, and fungi but absent from host cells. This gives the innate system broad but non-specific detection that requires no prior exposure.

Question 2

Fever is a harmful, uncontrolled side effect of immune activation that the body attempts to suppress.

• T. True
• F. False

Answer: False

Fever is an actively regulated, adaptive response. Cytokines (IL-1, IL-6, TNF-α) act on the hypothalamus to raise the body's thermostat. The elevated temperature impairs pathogen replication, enhances immune cell activity, and increases antibody production. It is a feature, not a bug, of the innate response — though extreme fever can itself become harmful.

Question 3

What is the functional difference between opsonization and the membrane attack complex in the complement cascade?

Model answer: Opsonization involves coating a pathogen surface with complement fragments (especially C3b) that phagocytes recognize via complement receptors, making the pathogen easier to engulf and destroy. The membrane attack complex (MAC) is a pore-forming assembly (C5b-C9) that directly inserts into pathogen membranes, causing lysis through uncontrolled ion and water flux.

The complement cascade has multiple effector outputs: C3b-mediated opsonization tags pathogens for phagocytosis, anaphylatoxins (C3a, C5a) recruit and activate immune cells, and the MAC directly destroys gram-negative bacteria. Understanding these as distinct mechanisms — rather than a single 'complement kills bacteria' outcome — clarifies why complement deficiencies have varied clinical consequences.