Ticks use 'tricks' to feed on human bodies without being detected

Ticks are small, but their saliva is busy. It carries a toolkit of proteins and other molecules that let a tick feed for days while keeping the bite site quiet and easy to tap for blood.

In the United States, an estimated 476,000 people are diagnosed and treated for Lyme disease each year, a figure that shows why this biology matters, according to a 2021 estimate.

A new scientific review maps out how these saliva components reshape the skin’s defenses, from the earliest minutes of a bite to the longer window when microbes can slip in.

The big idea is simple, and a little unsettling, because the tick’s spit changes how our immune system responds right where the mouthparts lock on.

After that overview, here is the lead researcher. Dr. Johanna Strobl of the Medical University of Vienna and CeMM Research Center for Molecular Medicine helped synthesize the latest findings and place them in a clear, practical frame for clinicians and the public.

Ticks have tricky saliva

Your skin’s first responders are built to move fast. The innate immune system is the immediate defense that jumps on injury and germs without needing a warm up or a memory from past infections.

Tick saliva meets it with proteins that block signals, thin the blood, and keep clotting at bay.

Many of those proteins have names worth knowing. Serpins are protease inhibitors that put brakes on enzymes that normally fan the flames of inflammation.

Cystatins block different enzymes that help immune cells process and present antigens. Together they slow cell recruitment and damp down the noise that would usually make a bite red and itchy.

Another family acts like a sponge for the body’s traffic signals. Chemokines are messenger proteins that tell immune cells where to go, and tick evasins bind them with high selectivity.

A 2008 report demonstrated that evasins can grab specific chemokine targets and stop immune cells from homing to the bite.

Tick saliva blunts the first response

A bite normally triggers neutrophils to swarm the site within minutes. Saliva proteins interfere with that rush by blocking chemokines, choking off platelet activation, and thinning local clots.

Less clotting means easier sipping, and less signaling means fewer alarm bells for nearby cells.

Tick proteins also tamper with complement, a set of blood proteins that assemble into complexes that punch holes in microbes.

By interrupting parts of the pathway that activate complement, saliva buys time for the tick, and for any passengers it carries. That includes proteins that mimic our own complement regulators to short circuit the system.

Platelet blocking matters as well. Saliva enzymes like apyrase degrade ADP that platelets use to clump, while Kunitz type inhibitors and serpins slow thrombin generation. Blood keeps flowing in the tiny space the tick creates, and the bite site stays calmer than it should.

How they quiet T-cells

The adaptive immune system would normally build a targeted response over hours to days. Saliva undercuts that by directly targeting helper T cells and the dendritic cells that activate them.

One important protein, Salp15, attaches to immune cells and blocks the signals they need to switch on and multiply.

A mechanistic study in 2006 showed that Salp15 physically associates with the CD4 receptor and suppresses T cell activation.

That single move weakens the handoff between dendritic cells and T cells and slows the building of a strong, lasting response at the skin.

Some saliva proteins tilt the immune response toward a type that is less effective at fighting many bacteria.

This shift weakens the defenses normally powered by other immune pathways, making it easier for certain microbes to take hold.

Microbes use tick saliva

When the local alarm is muted, microbes have a window to establish a foothold.

Borrelia burgdorferi, the Lyme bacterium, benefits from tick proteins that protect it from complement mediated killing in the skin. That protection helps more organisms survive the early hours after transmission.

A 2011 paper identified a lectin pathway inhibitor in tick saliva that blocks binding events needed to activate complement and recruit neutrophils. This single factor raised bacterial survival at the bite site and boosted transmission in animal models.

Chemokine binding by evasins adds another layer by limiting cell recruitment to the bite.

Fewer recruited dendritic cells can mean weaker T-cell priming, and lower antibody class switching downstream. The biology stacks up in the tick’s favor, and in the pathogen’s favor too.

From spit to medicine

The same features that make saliva useful to ticks could be repurposed to treat human disease. Evasins that soak up chemokines might someday help in conditions where runaway cell recruitment damages tissue.

Protease inhibitors from saliva are already being explored as topical tools against inflammatory skin disease.

“Just seconds after a tick bite, the animal releases its saliva into the host’s skin. The bioactive molecules it contains cause the blood vessels to dilate, inhibit blood clotting and suppress inflammatory reactions,” said Dr. Strobl.

The review also highlights vaccine ideas that target saliva rather than a single pathogen.

If a vaccine could make a tick’s bite inflame quickly and force detachment, it could reduce feeding time and lower the odds of transmission across the board.

Early animal studies with multicomponent saliva targets show signs that this path is plausible.

What to watch next

Better protein catalogs are coming from proteomics and transcriptomics of salivary glands across feeding stages.

Those data will sort out which molecules appear first, which persist, and how infections inside the tick change the saliva cocktail. That timing is central to which targets make sense for drugs or vaccines.

Work on extracellular vesicles and microRNAs is also growing. These tiny packets can carry regulatory signals from the tick into skin cells, and they probably rewire gene expression during a bite.

Understanding those signals could reveal non protein targets that are easier to stabilize as medicines.

Finally, keratinocytes and other structural skin cells deserve attention. They are not bystanders, they sense pathogens and broadcast signals that shape immunity and repair.

If tick saliva modulates their programs, that may explain why bites stay quiet and why wounds at the site can heal differently.

Next steps with tick saliva

For clinicians, these mechanisms explain why early local signs can be muted and why removal time matters.

The less time a tick has to feed, the less saliva it can pump in, and the fewer tricks it can use to tilt the odds. For public health, saliva targets offer a way to cut across the diversity of tick borne threats.

For researchers, saliva proteins are probes for the immune system. Each protein that blocks a pathway becomes a tool to test what that pathway does in real skin.

Those tools can also be starting points for drugs that need precision, not broad immunosuppression.

The study is published in Frontiers in Immunology.

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