Question textWhat am I? I am part of the innate immune system and confer some immunity to pathogens. I consist of a series of proteins that bind to the surface of a pathogen. Sometimes I can ‘punch holes’ in the cell wall / membrane of the pathogen to destroy it. Other times I can opsonise the pathogen and recruit phagocytes to destroy the pathogen. I am Answer 1 Question 18[select: , A pathogen associated molecular pattern (PAMP), A B cell, The complement system, A pathogen recognition receptor (PRR), An antibody].

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BlackTom AI · Accepted Answer

Here is the analysis of each option in the context of the described innate immune component.
Option 1: A pathogen-associated molecular pattern (PAMP). A PAMP is a molecular signature found on pathogens that is recognized by the immune system, not a component that directly performs actions like punching holes or opsonizing. So this choice misidentifies the effector mechanism described.
Option 2: A B cell. B cells are part of the adaptive immune system and produce antibodies; they are not the innate serum protein cascade that can form pores or opsonize directly. This option incorrectly assigns an adaptive cell type to a process that is typically innate and involves soluble proteins.
Option 3: The complement system. This option matches the description precisely: the complement system is a group of plasma proteins that, upon activation, can form membrane attack complexes that punch holes in pathogen membranes and can also opsonize pathogens (e.g., via C3b) to recruit phagocytes for destruction. It is a classic innate, protein-based defense mechanism.
Option 4: A pathogen recognition receptor (PRR). PRRs are innate receptors (like toll-like receptors) that detect PAMPs, but they are not the soluble proteins that form pores or mediate opsonization themselves. They initiate signaling, rather than performing the pore-formation or opsonization actions described.
Option 5: An antibody. Antibodies are part of the adaptive immune response and participate in opsonization and complement activation, but they themselves do not form the direct pore-forming actions described, nor are they the innate protein cascade; they work with the complement system or Fc receptors on phagocytes. Hence this is not the best match for the described innate, pore-forming, direct-action system.
In summary, option 3 correctly identifies the complement system as the innate cascade responsible for both forming pores in pathogens and promoting opsonization for phagocyte recruitment, while the other options refer to components or concepts that do not fit the described mechanism.

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