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If you have a population of T cells that are armed and ready to protect you, you could control the infection better than someone who doesnt have those cross-reactive cells, said Marion Pepper, an immunologist at the University of Washington who is studying the immune responses of Covid-19 patients. Thats what were all hoping for. T cells are an exceptionally picky bunch. Each spends the entirety of its life waiting for a very specific trigger, like a hunk of a dangerous virus. Once that switch is flipped, the T cell will clone itself into an army of specialized soldiers, all with their sights set on the same target. Some T cells are microscopic assassins, tailor-made to home in on and destroy infected cells; others coax immune cells called B cells into producing virus-attacking antibodies. The first time a virus infects the body, this response is sluggish; it takes several days for the immune system to sort out which T cells are best suited for the job at hand. But subsequent encounters typically prompt a response that is stronger and faster, thanks to a reserve force of T cells, called memory T cells, that lingers after the initial threat has passed and can quickly be called into action again. Usually, this process operates best when T cells must battle the same pathogen again and again. But these recruits are more flexible than they are often given credit for, said Laura Su, an immunologist and T cell expert at the University of Pennsylvania. Should these cells chance upon something that bears a strong resemblance to their germ of choice, they can still be roused to fight, even if the invader is a total newcomer. In theory, cross-reactive T cells can protect almost like a vaccine, said Smita Iyer, an immunologist at the University of California, Davis, who is studying immune responses to the new coronavirus in primates. Previous studies have shown that cross-reactive T cells may guard people against different strains of the
