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Viral infections activate their own appropriate PRRs. Some of these receptors respond to double-stranded RNA, which does not normally occur in human cells and therefore signals infection with an RNA virus.2 Double-stranded DNA does of course occur in human cells, but not normally in the cytosol. Its presence in that cellular compartment therefore signals infection with a DNA virus; and accordingly it, too, is detected by a suitable PRR.
Yet other types of PRRs respond to molecules which are normally present only within healthy body cells but which may be released from decaying dead cells. In the context of microbial infection, such “hidden self” signals are useful for amplifying the immune response. On the other hand, they can also contribute to autoimmune disease: once autoimmunity has passed a threshold beyond which it can destroy our own body cells, the hidden self signals released by those destroyed cells will further incite and sustain the autoimmune aggression.
Activation of cytotoxic T-cells. Once the non-specific re- sponse to an infection has set the stage, the specific immune response will begin. We will now consider how the appropriate antigen-specific T-cell and B-cell clones are selectively activated, beginning with the cytotoxic T-cells.
We had seen that, whenever a cell produces a protein, a sample of those protein molecules will be chopped up into small fragments that are transported to the surface of the cell, where they become amenable to interaction with and recognition by cytotoxic T-cells. Envisage the interaction between a cytotoxic T-cell and a presented protein fragment as one between lock and key (Figure 2.6). Our reservoir of cytotoxic T-cells contains myriad different locks (T-cell receptors), which can fit a virtually limitless variety of possible keys (fragments). Yet, the proteins of any given virus will only give rise to a limited number of keys, which will bind and activate only a correspondingly limited subset of all available cytotoxic T-cells.
Building your trust, by design