The researchers studied how the immune systems of the two mouse strains reacted to infection with Streptococcus pneumoniae, the bacterium that causes pneumonia. They found that the mice lacking B-1a cells were susceptible to infection, showing they lacked the natural antibodies of the innate immune system. Yet, these mice could be protected by immunization, which activated their adaptive long-term immune system.
By contrast, the mice with overproduction of CD19 and thus overproduction of B-1a cells did not achieve adaptive immunity as a result of vaccination.
Thus, the researchers concluded that the B-1a cells regulate the innate immune response and the B-1b cells regulate the adaptive, long-term immune response.
Said Haas, "This reciprocal contribution of these two subtypes of B-1 cells to innate and acquired immunity was surprising to us. No one knew much about what these subsets do.
Our results indicate that there is a tiered response system in which one kind of B-1 cell consistently provides a low level of protection, while the other specifically responds to an infection to help eliminate it."
According to Haas and Tedder, the findings offer potential insights into the mechanism of vaccine action. For example, the new insights into the roles of the two B-1 cell subtypes could help explain why the immune-triggering molecules called antigens from the pneumococcus bacteria do not elicit a strong adaptive immune response in infants, people with compromised immune systems and the elderly. Such people may
Contact: Dennis Meredith
Duke University Medical Center