Acquired tick resistance: The trail is hot

Abstract

Acquired tick resistance is a phenomenon wherein the host elicits an immune response against tick salivary components upon repeated tick infestations. The immune responses, potentially directed against critical salivary components, thwart tick feeding, and the animal becomes resistant to subsequent tick infestations. The development of tick resistance is frequently observed when ticks feed on non-natural hosts, but not on natural hosts. The molecular mechanisms that lead to the development of tick resistance are not fully understood, and both host and tick factors are invoked in this phenomenon. Advances in molecular tools to address the host and the tick are beginning to reveal new insights into this phenomenon and to uncover a deeper understanding of the fundamental biology of tick-host interactions. This review will focus on the expanding understanding of acquired tick resistance and highlight the impact of this understanding on anti-tick vaccine development efforts.

Keywords: Ixodes; acquired tick resistance; anti-tick vaccine; basophils; immune modulation.

Figure 1.. Hard tick attached to host skin and secreting pharmacologically active salivary components into the feeding lesion.

A. Ixodid ticks attach to the host skin by inserting their hypostome into the dermis of the host skin and adhere firmly with the help of salivary cement that is deposited at the bite-site and around the hypostome. Saliva secreted into the feeding lesion thwarts defense responses of the host. SG, salivary glands; Mc, macrophage; N, neutrophils; Lc, Langerhans cells; Dc, dendritic cells; E, eosinophils; Mt, mast cells; B, B-cells; L, lymphocytes; Cg, procoagulants; C, complement factors. B. Brief overview of predominant salivary functions characterized in tick saliva. Percent calculations based on the literature surveyed in this review.

Figure 2.. Potential mechanisms of acquired tick resistance.

Factors that may drive the dichotomous immune responses to tick bites on permissive or resistant host species include: Optimal (A) or suboptimal (A’) engagement of salivary proteins with host defense responses; genetic predisposition to decreased (B) or increased (B’) inflammatory responses to salivary proteins; structural and immunological differences in the skin (C, C’); Host-specific salivary proteome that is sufficient (D) or deficient (D’) in modulating host defense responses; and differences in wound healing without scar (E) or with scar (E’) formation.