When blood spills, the human body calls on platelets. These cells quickly plug the damaged region of a blood vessel and initiate clotting.
There’s more to platelets than clots, however. The bloodborne cells can also stimulate the immune system to adapt its response to a specific microbial assault, according to a report in the July Immunity.
“Most immunologists . . . think of platelets as these little things that induce coagulation. It will take time for them to realize the importance of platelets in modulating adaptive immunity,” says study coauthor Timothy L. Ratliff of the University of Iowa in Iowa City.
Indeed, the new work adds to a growing set of data indicating that platelets may have a significant role in immunity. For example, Michael Yeaman of the University of California, Los Angeles Medical Center and his colleagues have shown that platelets can release proteins that rapidly kill bacteria and some other microbes. “It’s no surprise that a cell that is adapted to navigating to wounds, where microorganisms would likely enter, also has several complementary host-defense functions,” says Yeaman.
In mammals, the immune reaction to a dangerous microbe comes in two stages. An initial counterattack, the innate response depends on patrolling cells such as macrophages and neutrophils, which recognize features common to many microbes. The second defense, the adaptive response, occurs as the immune system gradually ramps up production of T and B cells that specifically target the offending microbe. For example, the response boosts the number of B cells that make antibodies that bind to unique surface features of the microbe.
Yeaman and other investigators have found that platelets may participate in the innate immune response by killing microbes directly or by releasing inflammatory chemicals that beckon macrophages and neutrophils. The new study by Ratliff and his colleagues extends the influence of platelets to subsequent immune events.
In test-tube experiments, the scientists confirmed earlier reports that platelets can make a surface protein, called CD154, that regulates the adaptive immune response. For example, CD154 induces maturation of immune system components called dendritic cells, which in turn stimulate T- and B-cell growth.
Ratliff’s team showed that platelets bearing CD154 trigger dendritic-cell maturation when the two cell types are grown together. The researchers also found that a transfusion of CD154-bearing platelets into mice that can’t make CD154 influenced the rodents’ B cells and T cells. Among other effects, B cells began producing more of a certain class of antibodies.
Finally, Ratliff and his colleagues depleted other mice of most of their platelets and then injected the animals with a virus. These rodents produced significantly fewer antibodies to the virus than did mice with normal platelet counts.
According to John Semple of the University of Toronto, the new work could shed light on the rare cases in which the human immune system generates antibodies against its own platelets. “Platelet-derived CD154 may be the link that stimulates these pathogenic antibody responses,” he says.
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