Lyme Disease and Thymic Protein A

Lyme Disease and Thymic Protein ALyme disease acquired its name from Lyme, Connecticut, following an early outbreak of the disease among children in this town. Unique skin lesions (bulls-eye rash) are usually the first characteristic feature of infections.

Migrating redness, flu-like symptoms and arthralgia are often accompanying symptoms as well. This disease is caused by borrelia burgdorferi, a microscopic, spiral-shaped and highly mobile organism.  It is transmitted to humans through the bite of small ticks, as B. Burgdorgferi is transmitted in the saliva of ticks. Individuals active in wooded areas need to take special precautions against tick bites for this reason.

The thymus gland plays a key role in defending the body from B. Burgdorgferi . Specialized cells, known as B-cells, mature in critical regions of the thymus and produce a class of antibodies known as Immunoglobin-type G and type M (IgG and IgM).  Through B-cells, the thymus produces IgM to protect against all foreign species that attempt to colonize within the body. However on detecting a foreign invader, IgM recruits T-cells and other immune cells to surround and wall-off the organism. IgG in particular is able to bind tightly to foreign antigens and provide a docking station for stronger immune cells to attach and lyse B. Burgdorgferi.

Additionally, specific T-cells, known as CD4+ T cells transports foreign particles back to the thymus and present them to immature B-cells here, which immediately mature and produce immunoglobulin type G, specifically able to target the invader for breakdown. This response can expand from months to years and provides lasting protection against the organism, as the thymus continues to produce specific antibodies, in order for the body to immediately recognize and respond to future invasion.