Unlike the current US congress, different parties in the immune system engage in useful conversation. Thus, when the adaptive immune system (party) is overstimulated, as can occur with persistent virus infection, ways are needed to dampen such events without messing up the whole system. One mechanism to achieve this objective was recently described in Immunity {1}. The mechanism involves a protein, pros1, that is expressed by activated T cells, and which acts as a ligand for the receptor tyrosine kinase TAM expressed by dendritic cells (DCs; innate immune party members). Engaging TAM dampens the activity of DCs, which includes their proinflammatory and effective antigen presentation function. One outcome is curtailment of further T cell activation and selective dampening of an over-stimulated host-damaging situation.



It turns out that this otherwise useful homeostatic feedback mechanism can be exploited by some crafty viruses as a countermeasure against host control, as reported in Cell Host & Microbe {2}. Accordingly, some enveloped viruses, such as the increasingly troublesome flaviviruses Dengue and West Nile fever, express phosphatidylserine on their outer coats. This permits such viruses to bind to the TAM ligands pros1 and gas6 with the complex triggering TAM-expressing cells such as DCs to stop producing the useful antiviral protein interferon type 1. Thus, some viruses can act like members of the Tea Party and disrupt an otherwise functioning congress solely for their own benefit.