A protein used by the body for dampening down type I interferon (IFN-I) - a major anti-viral factor - is reported online this week in Nature Immunology. Such fine-tuning of IFN-I expression is necessary to avoid the overproduction of the anti-viral factor which can trigger development of autoimmune diseases, such as psoriasis and systemic lupus erythematosus.
Young-Joon Kim and colleagues demonstrate that OASL1, a protein found inside certain immune cells, strongly suppresses the production of IFN-I. Accordingly, mice lacking OASL1 are exceptionally resistant to infection by certain viruses. They suggest that OASL1 operates by inhibiting the activation of IRF7 - a protein responsible for switching on IFN-I production. OASL1’s mechanism of action is highly peculiar; it doesn’t inhibit the IRF7 protein, rather it specifically recognizes a unique 3-dimensional motif of IRF7’s mRNA and prevents it from being translated into protein.
Although many other studies have identified mechanisms to control immune responses relatively few have focused on this fundamental anti-viral pathway nor identified an equivalent system to regulate mRNA translation so specifically.