Final answer:
NK cells can become cytotoxic through various mechanisms induced by inflammatory cytokines. CD94:NKG2A on NK cells recognizes HLA-E on target cells and acts as a go, no-go signal.
Step-by-step explanation:
NK cells arise from the innate immune system but play a key role in innate immune responses to viral infection. Inflammatory cytokines can make NK cells cytotoxic through three different ways:
- By inducing the expression of the Fas ligand on the surface of NK cells, which can bind to the Fas molecule on the target cell, triggering apoptosis.
- By secreting perforin, a protein that creates pores in the target cell's membrane, allowing entry of other cytotoxic molecules into the cell.
- By releasing granzymes, proteases that can enter the target cell through the pores created by perforin and induce apoptosis.
CD94:NKG2A is a receptor on the surface of NK cells that recognizes HLA-E, a molecule expressed by healthy cells. When CD94:NKG2A binds to HLA-E, it acts as a go signal, signaling the NK cell not to kill the healthy cell. However, when the expression of HLA-E is downregulated, for example, during viral infection, CD94:NKG2A cannot bind to it, indicating a no-go signal and allowing NK cells to kill the infected cell.