Unlike most static cells in the body, immune cells constantly migrate through environments that vary considerably both in steady state and during invasion by a pathogen. The unpredictability of these environments can be thought of as a selective force that through evolution has favored substantial population diversity in cells of the immune system.

Diversification can happen at the level of DNA (through recombination or mutation) to produce, for example, novel receptors on B cells, than can better deal with pathogens. Not surprisingly, similar types of processes also occur in pathogens, for the purposes of evading a targeted immune response (and we will discuss the African trypanosome as an example of that).

But diversification can also happen at the level of RNA. This type of transcriptomic diversity is generated by robust and targeted RNA editing (an "active" form of mutation, which depends on concurrent expression of the editing deaminases of the APOBEC or ADAR families, and which unlike DNA mutation does not leave a mark on the genome). We will discuss mechanisms by which editing affects the proteomic output of the cell, and the functional relevance of editing for immune cells, both at the steady state, and in disease contexts.