"After resolution of a viral infection we want to have ASCs in our lungs to guard our mucosal surfaces, the port of microbial entry, in case of a reinfection with the same virus," Wolf said. "The lung microenvironment after a viral infection allows the ASCs to persist as a sort of local base, a place for the local release of protective antibodies."
"To avoid damage of the lung tissue, the immune system wisely evolved means of keeping the secretion of antibodies under tight control," Wolf explained. "The anti-viral ASCs in the lungs are short-lived and require BLyS and APRIL for their more immediate survival, but also the generation of longer-lived ASCs that take up residence in the bone marrow depends on these signals."
According to Wolf, it might be possible to manipulate ASC behavior to prolong or strengthen the effectiveness of vaccines. Drugs that induce targeted production of ASC survival factors, such as BLyS and APRIL or manipulation of their signals through TACI, their receptor, could theoretically help to maintain specific antibodies. While the seasonal flu is constantly mutatingnecessitating an annual vaccine even weakly reactive antibodies could be protective if there are enough of them and if their production is sustained.
One interesting observation from this study, the researchers say, is that the persistence of ASCs in different tissues appears to be regulated differently. This has spurred plans for the Erikson laboratory to conduct a genome-wide molecular survey in collaboration with Wistar Professor Louise Showe, Ph.D., director of Wistar's genomics facility.
|Contact: Greg Lester|
The Wistar Institute