2019 Jan 22. doi: 10.1097/DAD.0000000000001352. [Epub ahead of print]

A Reactive Peripheral Gamma-Delta T-cell Lymphoid Proliferation After a Tick Bite.


Peripheral gamma-delta T-cell proliferations are encountered in reaction to certain infections and in primary malignancies. Identifying sources of benign reactions is key in avoiding unnecessary workup and surveillance of these aggressive malignancies. Borrelia infections have been implicated in a number of lymphoproliferative disorders, but rarely, if ever, in this setting. While gamma-delta T-cells are known to play a prominent role in the immune response to Borrelia infection, B-cell differentiation is encountered in the majority of Borrelia-associated proliferations. We present here a unique case of benign-appearing peripheral gamma-delta T-cell lymphoid proliferation in the setting of a tick-bite with subsequent erythema migrans-like skin findings.



Again, nobody has a clue as to whether this is “unique” or not due to faulty antibody tests that are missing over half of all Lyme cases.  So many patients are flying under the radar and nobody’s looking.  Again, many don’t present with the EM rash.

Many say this T-cell proliferation is perhaps more common than thought.

The investigators now think they know how it’s happening. They have identified a T cell receptor that interacts with surface molecules on B. burgdorferi. According to the study, this interaction causes bystander activation of T cells, which in turn causes the T cells to produce inflammatory molecules that lead to arthritis symptoms around the joints.

Those activated T cells can continue to interact with residual bacteria long after the initial tick bite, meaning some patients continue to feel symptoms like arthritis…

They realized that T cells in the mice were undergoing bystander activation. “Instead of activating a very small, specific set of T cells, it causes this global activation of immune cells,” Ms. Whiteside said. Once activated, those T cells can interact with residual bacteria to generate continued inflammation even long after the initial infection.

Research possibilities are endless, yet most researchers either get hung up on climate change or fixate on the acute phase of Lyme.