Researchers at National Jewish Health have discovered a trigger that induces B cells to produce effective and long-lived antibodies early in the immune response. They found that a molecule that binds toll-like receptors (TLR) doubles the early antibody response to an antigen, and shifts it to a more effective, IgG form.
The findings, published online and in the July 5, 2010, issue of the Journal of Experimental Medicine, support the emerging concept of 'bridge immunity,' which links the innate and adaptive arms of the immune response. They may also lead to the development of better vaccines.
"In our experiments, a molecule that interacts with the innate immune system stimulates follicular B cells, which are recognized as part of the adaptive immune system," said senior author Raul Torres, PhD, Associate Professor of Immunology at National Jewish Health. "Our data provide evidence of a continuous immune response, rather than two distinct and separate arms."
A gap in the immune response?
The innate immune response begins within minutes to hours after an infection begins by recognizing general molecular patterns associated with infectious organisms, such as components of bacterial cell walls. It is rapid but not particularly focused. The adaptive immune response detects proteins associated with specific invaders, and ultimately produces highly targeted antibodies that help neutralize foreign organisms. That process begins several days after the infection has begun, and does not reach full strength for 10 days to two weeks on average.
For many years, scientists thought the two arms of the immune response acted separately and independently. If that were true, however, there would be a gap in protection after the innate response fades and before the adaptive response kicks in. In recent years, scientists have begun realizing that the two arms of the immune system communicate with each other to fill that gap.
|Contact: William Allstetter|
National Jewish Health