Published online before print November 13, 2009
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||

,2
* Cancer Immunology Program, Peter MacCallum Cancer Centre, East Melbourne, Victoria, Australia; and Departments of
Microbiology and Immunology and
Genetics, The University of Melbourne, Victoria, Australia
2. Correspondence: Peter MacCallum Cancer Centre, Cancer Immunology Program, St. Andrews Place, East Melbourne, Victoria 3002, Australia. E-mail: ilia.voskoboinik{at}petermac.org
A pore-forming protein, PRF, and serine proteases, Grz, are key effector molecules of CL. These toxins are stored within secretory granules, which exocytose their contents in response to immune synapse formation between the CL and virus-infected or transformed target cell. There, PRF and Grz synergize to induce various apoptotic death pathways and to maintain immune homeostasis. Mechanistic aspects of the synergy and apoptotic mechanisms are still not fully understood, and the current review will address some of the hotly debated controversies in the field.
Key Words: cytotoxic lymphocyte natural killer cell familial hemophagocytic lymphohistiocytosis