Centre for Cancer Research News

Zinc Finger Protein Key to Immune Response

A new paper published online in the prestigious journal Immunity, presents the results of a research project led by Professor Bryan Williams.

The paper describes the discovery that promyelocytic leukemia zinc finger protein (PLZF) plays an important role in the immune response mediated by interferon. Interferon is shown to stimulate an association between PLZF and cofactors to switch on several key interferon-stimulated genes, including those involved in protection against viral infections.

Interferon is a naturally produced substance that modulates the innate immune response and provides protection against viral infections and cancer. It has been developed for clinical use over many years, and has been used in the treatment of hepatitis, cancer and autoimmune diseases, such as multiple sclerosis. Although much has been learned about the mechanism of action of interferon, the reason that some patients are more sensitive to treatment with interferon than others has proved difficult to identify.

The study found mice lacking the gene that codes for PLZF are found to be more susceptible to infection with viruses. In addition, the activity of natural killer cells, which play an important role in the innate immune response, is impaired in mice lacking PLZF.

The results described in the study provide new insights into the mechanisms regulating the action of interferon, and demonstrate that PLZF is an important factor in the immune response and could therefore be used as a possible drug target for both anti-viral and anti-tumour drug therapy.

The paper can be found online at http://www.cell.com/immunity/home   

A preview, by Professor Keiko Ozato, of this important paper appears in the same issue of Immunity. 

Illustration:
Interferons interact with receptors on the cell surface to initiate signalling processes that result in the activation of interferon-stimulated genes within the nucleus. We have identified PLZF as a novel component of the interferon response, which activates many interferon-stimulated genes.