Volunteer for NIAID-funded clinical studies related to Lyme disease on ClinicalTrials.gov.
The results of recent studies conducted by NIAID and intramural scientists from the National Institute of Neurological Disorders and Stroke indicate that T cells from patients with chronic Lyme disease are reactive not only against Borrelia burgdorferi-specific antigens but also against various host (self) antigens (Nature Med, 5:1375, 1999). Such antigenic mimicry might generate autoimmune inflammatory reactions that could be responsible for arthritic as well as some neurological symptoms associated with chronic Lyme disease. Intramural and extramural scientists are exploring the implications of this finding.
Antibodies against the OspA epitopes of B. burgdorferi also have been shown to cross react with neural tissue (J Peripheral Nervous System. 9:165, 2004; J Neuroimmunol. 159:192, 2005) as well as myocin (J Clin Microbiol. 43:850, 2005). Such antigenic mimicry may have the potential to generate autoimmune inflammatory reactions that could be responsible for the neurological symptoms associated with chronic Lyme disease. Intramural and extramural scientists are evaluating this possibility in greater detail. In this context, it is interesting to note that homologies between proteins of B. burgdorferi and thyroid antigens also have been reported (Thyroid. 14:964, 2004).
In clinical studies conducted by NIAID-supported extramural scientists, case subject patients with post-treatment chronic Lyme disease (PTCLD) were compared to control subjects without such symptoms for the presence of several human leukocyte antigen (HLA) class II (DRB1 and DQB1) genetic markers, some of which are known to be associated with the expression of autoimmune reactivity. The results obtained did not support the involvement of an autoimmune mechanism in PTCLD (J Infect Dis. 192:1010, 2005). However, since not all autoimmune diseases are associated with specific HLA haplotypes, these findings do not necessarily exclude that possibility. Definitive proof clearly would involve demonstrating the presence of significant levels of relevant autoimmune antibodies and/or autoreactive T cells in patients with PTCLD, but not in treated control subjects without such symptoms. A greater frequency of DRB1*0401, which has been reported to be associated with antibiotic-treatment resistant arthritis (Science. 281:703, 1998) was noted in the case subject patients. Although this finding appeared to be nominally significant (p <0.05), its biological significance is ambiguous since none of the case subjects considered had symptoms of inflammatory arthritis.
back to top
Last Updated December 05, 2007
Last Reviewed December 05, 2007