The ability of B. burgdorferi, the spirochete responsible for Lyme Arthritis, to avoid clearance by the immune system may be attributed in part to an inadequate innate immune response upon infection. However, innate cells such as monocytes, macrophages, and dendritic cells display a vigorous response against borrelial infection and play a major role in the activation of the adaptive immune response against the spirochete. Despite these efforts, though, arthritis still develops in a significant number of patients infected with B. burgdorferi. It appears that the robust response elicited by monocytes, macrophages, and dendritic cells against the spirochete may be viewed as insufficient in early infection but excessive in the later stages. Paradoxically, in mounting such a strong defense against the organism, these cells may inadvertently be contributing to the induction of Lyme arthritis.
Lyme disease is associated with a chronic inflammatory bias with excessive T helper 1 cytokines. This condition has responded to PURSOR therapy in a Rhode Island lady who had not responded to antibiotic treatment at Yale under the care of my medical school classmate Allen Steere who has deservedly earned a reputation in this field.
Lyme Arthritis: Current Concepts and a Change in Paradigm