Lyme disease, caused by the spirochete Borrelia burgdorferi (Bb), is the most common vector-borne illness in the United States. It is a complex disease that may affect the skin, joints, heart, eyes, and central nervous system. Prompt diagnosis and treatment are curative in most instances. However, a significant percentage of patients experience ongoing symptoms after treatment. Currently, there is much controversy regarding the diagnosis, pathophysiology, and treatment of Lyme disease.
Many believe the ongoing symptoms are due to factors such as autoimmunity or permanent damage incurred during the active infection.
The immunomodulation 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 immunomodulation and prevent or improve chronic musculo-articular damage.
The control of the REDOX system favors the immunological balance between cytotoxic cells and regulatory cells.
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