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 feeding 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 the agent of Lyme disease, Ixodes dammini, profoundly inhibited splenic T cell proliferation in response to stimulation with concanavalin A or phytohemagglutin, in a dose-dependent manner. In addition, interleukin 2 secretion by the T cells was markedly diminished by saliva. Tick saliva also profoundly suppressed nitric oxide production by macrophages stimulated with lipopolysaccharide. Finally, we analyzed the molecular basis for the immunosuppressive effects of saliva and discovered that the molecule in saliva responsible for our observations was not PGE2, as hypothesized by others, but rather, was a protein of 5,000 mol wt or higher.
Article|
September 01 1994
Saliva of the Lyme disease vector, Ixodes dammini, blocks cell activation by a nonprostaglandin E2-dependent mechanism.
S Urioste,
S Urioste
Department of Tropical Public Health, Harvard School of Public Health, Boston, Massachusetts 02115.
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L R Hall,
L R Hall
Department of Tropical Public Health, Harvard School of Public Health, Boston, Massachusetts 02115.
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S R Telford, 3rd,
S R Telford, 3rd
Department of Tropical Public Health, Harvard School of Public Health, Boston, Massachusetts 02115.
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R G Titus
R G Titus
Department of Tropical Public Health, Harvard School of Public Health, Boston, Massachusetts 02115.
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S Urioste
Department of Tropical Public Health, Harvard School of Public Health, Boston, Massachusetts 02115.
L R Hall
Department of Tropical Public Health, Harvard School of Public Health, Boston, Massachusetts 02115.
S R Telford, 3rd
Department of Tropical Public Health, Harvard School of Public Health, Boston, Massachusetts 02115.
R G Titus
Department of Tropical Public Health, Harvard School of Public Health, Boston, Massachusetts 02115.
Online ISSN: 1540-9538
Print ISSN: 0022-1007
J Exp Med (1994) 180 (3): 1077–1085.
Citation
S Urioste, L R Hall, S R Telford, R G Titus; Saliva of the Lyme disease vector, Ixodes dammini, blocks cell activation by a nonprostaglandin E2-dependent mechanism.. J Exp Med 1 September 1994; 180 (3): 1077–1085. doi: https://doi.org/10.1084/jem.180.3.1077
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