Discovery May Make Vaccines More Potent
A new medical
study may help explain why certain vaccines often fail to generate protective
immunity against deadly bacterial infections.
Researchers
at Memorial Sloan-Kettering Cancer Center in New York hope their discovery
will result in more effective vaccines against not only microbes, but cancer
as well.
"We are targeting
bacterial infections where vaccine development has not been as effective
as we might wish, such as tuberculosis, salmonella and malaria," explained
senior researcher Eric Pamer, chief of infectious disease service at Memorial
Sloan-Kettering.
"We hope that
the mechanisms we're analyzing will potentially help optimize vaccine effectiveness."
Vaccines are
designed to provoke the body into developing an immunity against a specific
disease. They often are made with dead or impaired versions of whatever
causes the illness in question.
Vaccines using
killed or inactive germs are naturally considered safer than those that
use living but weakened microbes. However, "it's been known for decades
that vaccines made with killed bacteria are notoriously ineffective at
generating protective immunity," Pamer noted in an interview with United
Press International.
When a live
vaccine is introduced into the body, it stimulates production of key immune
system components known as effector T cells, which trigger a massive counter
attack against a disease.
While most of
these cells eventually die, about one out of 20 proceed to become memory
T cells, which remain in the body for months or even years. When the body
encounters the invader again, the memory cells rapidly generate new effector
T cells that stop the disease before it even starts.
Scientists
until now believed killed vaccines failed to generate memory cells, which
would explain their ineffectiveness. Pamer and his colleagues discovered
killed vaccines do trigger memory cell production, in large amounts. However,
the memory cells activated by killed vaccines curiously do not generate
effector cells when faced with new infections.
"That was quite
surprising," said immunologist Michael Bevin at the University of Washington
in Seattle, who reviewed the findings for Science magazine. "Another part
of their findings that was surprising, where both the live and dead form
of a vaccine were given to the same animal, suggested that the two may
even perform independently."
Pamer feels
that this new discovery suggests, "there is a switch that isn't turned
on by killed bacteria but is turned on by live bacteria. If we can flip
this switch on with killed vaccines, they can go on to kill bacteria."
These findings
may also aid cancer vaccine research, Pamer told UPI.
"One of the
problems with the development of vaccines that target tumors is optimizing
the function of the T cells, preventing them from losing their effector
functions," he explained. "We think our work has implications for the development
of more potent vaccines targeted at cancer."
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