Abstract
Ixodes ticks are the main vectors for a number of zoonotic diseases, including Lyme disease. Ticks secrete saliva directly into a mammalian host while feeding on the host's blood. This action serves to modulate host immunity and coagulation, thus allowing ticks to attach and feed upon their host. One of the most extensively studied components of tick saliva is Salp15. Research has shown that this protein binds specifically to CD4 molecules on the surface of T lymphocytes, interferes with TCR-mediated signaling transduction, inhibits CD4+ T cell activation and proliferation, and impedes the secretion of interleukin 2 (IL-2). Salp15 also binds specifically to dendritic cell dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN) to up-regulate the expression of CD73 in regulatory T cells. Collectively, these findings render this salivary protein a potential candidate for a range of therapeutic applications. Here, we discuss our current understanding of Salp15 and the mechanisms that might be used to treat disease.
Highlights
Mosquitoes and ticks are considered the most predominant vectors for the transmission of various pathogens to humans and animals [1, 2]
We describe our current understanding of Salp15 and discuss its role in pathogen-vector-host interactions
A recent study used bioinformatics analysis to predict post-translational modifications of Salp15 and its homologs; the results suggested that all Salp15 family members contain at least two N-linked glycosylation sites [25]
Summary
Mosquitoes and ticks are considered the most predominant vectors for the transmission of various pathogens to humans and animals [1, 2]. The effect of Salp on TCR signaling impedes the phosphorylation of PLC-γ1 downstream and leads to a significant reduction in calcium flux during the activation of CD4+ T cells [62] A recent study confirmed that Salp can bind to DCSIGN as a direct result of structures created by mannose and galactose This interaction inhibits the TLR-induced production of the pro-inflammatory cytokines IL-12, IL-6, and TNF-α by DCs and reduces the ability of DCs to activate T lymphocytes [19]. Because Salp can inhibit the proliferation of CD4+ T cells and the production of IL-2, it can hinder T cell-dependent IgG and IgE production and may serve as a potential target for suitable dermatological treatments
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