Antibodies themselves do not directly kill cells or pathogens in most cases. Their primary roles are neutralization (binding to toxins or pathogens to block their activity/entry) and opsonization (coating pathogens to enhance phagocytosis).
However, antibodies can trigger "killing" mechanisms when bound to antigens, particularly on cell surfaces, by activating other components of the immune system:
1.
Complement System Activation (Option d): Certain antibodies (IgM and some IgG subclasses), when bound to antigens on a cell surface, can activate the classical pathway of the complement system. Activated complement components can:
- Form a Membrane Attack Complex (MAC) that creates pores in the target cell membrane, leading to cell lysis (killing).
- Act as opsonins (C3b) to enhance phagocytosis.
- Promote inflammation.
This is a major way antibodies can lead to cell killing.
2.
Antibody-Dependent Cell-mediated Cytotoxicity (ADCC): Cells like Natural Killer (NK) cells have Fc receptors that can bind to antibodies (typically IgG) coated on a target cell. This binding activates the NK cell to release cytotoxic granules that kill the target cell.
Let's look at other options:
(a) Cytokines: Signaling molecules that modulate immune responses. They don't directly make an antibody a "killer" by binding to it. Antibodies can influence cytokine production.
(b) Interleukins: A type of cytokine.
(c) Chemokines: A type of cytokine that directs cell migration.
Among the options, binding of an antibody (to an antigen on a target) and subsequent activation of the
complement system is a direct way an antibody can lead to the killing/lysis of the target cell.
ADCC is another mechanism, but "Complement" is listed as an option.
So, when an antibody is bound to an antigen (e.g., on a bacterial cell) and then binds/activates complement, the complement cascade can lead to lysis of the cell.
\[ \boxed{\text{Complement}} \]