Thus, ADCC appears to be one of the most important immune effector functions.
Macrophages are the most important immune effector cells during the earliest stage of trauma and are activated by recognizing pathogen-associated molecular patterns (PAMPs) during the immune-defense reaction against infection.
In other instances, the soluble IL-6Rα (sIL-6Rα) subunit could often present itself as a soluble molecule, to form many IL-6/sIL6Rα complexes first, which are in turn attracted to two gp130 molecules (homodimers) expressed on most of the key immune effector cells including CD4+, CD8+ (CTLs), antigen presenting cells, and NK cells.
The innate immune effector cells, most notably macrophages, play a significant role in the defense against foreign bodies and the formation of a fibrous capsule around synthetic implants.
Since in our experiments the Tip-DCs turned out to be the most strongly infected cell population and the IFNβ+ Tip-DCs show a higher capacity to produce TNF and iNOS one could speculate that these IFNβ secreting cells are the terminally differentiated most potent cytokine producing innate immune effector cells.
The decrease in ADCC activity mediated by scIgG-T was consistent with its reduced binding affinity to FcγRs expressed on immune effector cells, most notably the loss of binding to FcγRIIIa that is known for its contribution to ADCC and is the main FcγR expressed on NK cells.
Yet, most tumors are not eliminated by immune effector cells, possibly because of the incompletely understood mechanisms of immune tolerance.
However, most of what is known about invertebrate immunity has been restricted to immune effector cells and little information is available on the immune responses of other tissues or organs.
Glycoengineering and other modifications of antibodies to enhance their immune effector functions appear, therefore, to be a most effective way to improve the efficacy of naked antibody therapy by a variety of mechanisms.
One of the most promising clinical applications of bispecific technologies is the redirection of immune effector cells to kill tumor cells.
