Antibody Dependent Cell Mediated Cytotoxicity
Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC) is a mechanism of cell-mediated immunity whereby an effector cell of the immune system actively lyses a target cell that has been bound by specific antibodies. It is one of the mechanisms through which antibodies, as part of the humoral immune response, can act to limit and contain infection.  Classical ADCC is mediated by natural killer (NK) cells; monocytes and  eosinophils can also mediate ADCC. For example Eosinophils can kill certain parasitic worms known as helminths through ADCC. ADCC is part of the adaptive immune response due to its dependence on a prior antibody response.

# ADCC by NK cells
The typical ADCC involves activation of NK cells and is dependent on the recognition of antibody-coated infected cells by Fc receptors on the surface of the NK cell.  The Fc receptors recognize the Fc (crystalline) portion of antibodies such as IgG, which bind to the surface of a pathogen-infected target cell.  The most common Fc receptor that exists on the surface of NK Cell is called CD16 or FcRIII. Once bound to the Fc receptor of IgG the Natural Killer cell releases cytokines such as IFN-, and cytotoxic granules containing perforin and granzymes that enter the target cell and promote cell death by triggering apoptosis. This is similar to, but independent of, responses by cytotoxic T cells (CTLs).

# ADCC by eosinophils
Large parasites like helminths are too big to be engulfed and killed by phagocytosis. They also have an external structure or integument that is resistant to attack by substances released by neutrophils and macrophages.  However, these parasites can become coated with an antibody called IgE that is recognized by an Fc receptor (FcRI) of eosinophils, a cell type that contains granules (such as major basic protein) against which helminths are not resistant.  The interaction of the FcRI receptor with the Fc portion of helminth bound IgE causes the eosinophil to release these granules in a mechanism similar to that of the NK cell during ADCC.

# Further reading
- Janeway CA, Jr.;  et al. (2001). Immunobiology (5th ed. ed.). Garland Publishing. (electronic full text via NCBI Bookshelf) ISBN 0-8153-3642-X.CS1 maint: Explicit use of et al. (link) CS1 maint: Extra text (link) .mw-parser-output cite.citation{font-style:inherit}.mw-parser-output q{quotes:"\"""\"""'""'"}.mw-parser-output code.cs1-code{color:inherit;background:inherit;border:inherit;padding:inherit}.mw-parser-output .cs1-lock-free a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-limited a,.mw-parser-output .cs1-lock-registration a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-subscription a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration{color:#555}.mw-parser-output .cs1-subscription span,.mw-parser-output .cs1-registration span{border-bottom:1px dotted;cursor:help}.mw-parser-output .cs1-hidden-error{display:none;font-size:100%}.mw-parser-output .cs1-visible-error{display:none;font-size:100%}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration,.mw-parser-output .cs1-format{font-size:95%}.mw-parser-output .cs1-kern-left,.mw-parser-output .cs1-kern-wl-left{padding-left:0.2em}.mw-parser-output .cs1-kern-right,.mw-parser-output .cs1-kern-wl-right{padding-right:0.2em}
- Pier GB, Lyczak JB, Wetzler LM (2004). Immunology, Infection, and Immunity. ASM Press. ISBN 1-55581-246-5.CS1 maint: Multiple names: authors list (link)