Lyme Disease

Lyme disease, caused by the spirochete bacterium Borrelia burgdorferi (Bb), is the most prevalent vector-borne illness in the United States, transmitted primarily through the bite of infected black-legged ticks. It is a multifaceted disease that can affect various systems in the body, including the skin, joints, heart, eyes, and central nervous system. Early diagnosis and prompt treatment with antibiotics are typically curative in most cases. However, a notable percentage of patients continue to experience persistent symptoms even after standard treatment, leading to ongoing discomfort and health challenges. This has sparked significant controversy and debate within the medical community, especially concerning the diagnosis, underlying pathophysiology, and appropriate long-term management of Lyme disease.

Cellular Immunotherapy for Chronic Lyme Inflammation

Many believe the ongoing symptoms are due to factors such as autoimmunity or permanent damage incurred during the active infection.

The immunomodulator caused by Bordetella depends on the activation or inactivation of regulatory T lymphocytes and natural killer (NK) lymphocytes; the imbalance of both causes the persistence of symptoms in the disease.

Proinflammatory cytokines increase in the joints, nervous, and cardiovascular systems, causing signs of chronic inflammation.

On the other hand, the dysregulation of T reg lymphocytes causes an increase in anti-inflammatory cytokines, which causes failure in the antibiotic treatment of these patients in the acute phase.

Knowing the levels of pro-inflammatory and anti-inflammatory cytokines, Treg lymphocytes and natural killer lymphocytes is convenient for designing personalized therapy in these patient groups.

Cellular immunotherapy’s objective in this group of diseases is to control immunomodulator and prevent or improve chronic muscle-articular damage.

The control of the REDOX system favors the immunological balance between cytotoxic cells and regulatory cells.