SALIVA OF THE LYME-DISEASE VECTOR, IXODES-DAMMINI, BLOCKS CELL ACTIVATION BY A NONPROSTAGLANDIN E(2)-DEPENDENT MECHANISM

Tick-borne pathogens would appear to be vulnerable to vertebrate host immune responses during the protracted duration of feeding required by their vectors. However, tick salivary components deposited during fee ding may inhibit hemostasis and induce immunosuppression. The mode of action and the nature of immunosuppressive salivary components remains poorly described. We determined that saliva from the main vector of t he agent of Lyme disease, Ixodes dammini, profoundly inhibited splenic T cell proliferation in response to stimulation with concanavalin A o r phytohemagglutin, in a dose-dependent manner. In addition, interleuk in 2 secretion by the T cells was markedly diminished by saliva. Tick saliva also profoundly suppressed nitric oxide production by macrophag es stimulated with lipopolysaccharide, Finally, we analyzed the molecu lar basis for the immunosuppressive effects of saliva and discovered t hat the molecule in saliva responsible for our observations was not PG E(2), as hypothesized by others, but rather, was a protein of 5,000 me l wt or higher.