Natural killer cells and interferon কী?

Viruses hide inside cells, where complement and phagocytes cannot reach them. Natural killer cells patrol for cells that have stopped displaying MHC class I — the “missing self” of a cell whose viral or tumour occupant has switched off antigen presentation to escape T cells (Chapter 16) — and for stress proteins that infected and transformed cells put on their surface; inhibitory receptors for MHC I and activating receptors for the stress ligands are summed, and a cell that tips the balance is killed within minutes by perforin and granzymes injected into it, which trigger its apoptosis. Type I interferons ($\alpha$ and $\beta$) are made by any cell whose RIG-I or cGAS has detected viral nucleic acid; secreted, they bind receptors on neighbouring cells and, through the JAK–STAT pathway, induce hundreds of genes that put those cells into an antiviral state: a kinase that shuts down translation when it meets double-stranded RNA, a nuclease that degrades RNA, proteins that block viral entry and assembly, and more MHC I to show T cells what is inside. The cell that made the interferon may die; its neighbours are forewarned. Interferon was discovered by Isaacs and Lindenmann (1957) as the factor in the medium of virus-infected cells that made fresh cells resistant, and it is the reason a cell infected by one virus resists a second.