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Cutting Edge: Immunity against a "Silent" Salivary Antigen of the Lyme Vector Ixodes scapularis Impairs Its Ability to Feed¹

Michalis Kotsyfakis^2,*, Jennifer M. Anderson, John F. Andersen^*, Eric Calvo^*, Ivo M. B. Francischetti^*, Thomas N. Mather, Jesus G. Valenzuela and José M. C. Ribeiro^*

^* Vector Biology Section and Vector Molecular Biology Unit, Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852; and Center for Vector-Borne Disease, University of Rhode Island, Kingston, RI 02881

Ixodes scapularis ticks transmit the Lyme disease agent in the United States. Although strong antitick immunity mediates tick rejection by certain vertebrates, only a few Ags have been molecularly characterized. We show that guinea pig vaccination against a secreted tick salivary immunomodulator, sialostatin L2, can lead to decreased feeding ability of I. scapularis nymphs. Increased rejection rate, prolonged feeding time, and apparent signs of inflammation were observed for nymphs attached to vaccinated animals, indicating a protective host immune response. Interestingly, sialostatin L2 humoral recognition does not take place upon repeated tick exposure in control animals, but only in the vaccinated animals that neutralize sialostatin L2 action. Therefore, we demonstrate an essential sialostatin L2 role upon nymphal infestation that can be blocked by vertebrate immunity and propose the discovery of similarly "silent" Ags toward the development of a multicomponent vaccine that will protect against tick bites and the pathogens they transmit.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by the Intramural Research Program of the Division of Intramural Research, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), and was also partially supported by NIH Extramural Grant 2R01AI37230 to T.N.M.

² Address correspondence and reprint requests to Dr. Michalis Kotsyfakis, Vector Biology Section, Laboratory of Malaria and Vector Research, 12735 Twinbrook Parkway, Rockville, MD 20852. E-mail address: mkotsyfakis{at}mail.nih.gov

³ The online version of this article contains supplemental material.