Lyme disease sucks worse than the tick that bit me...$0$0$0$0$0The Role of Autoimmune Reactivity$0$0The results of recent studies conducted by NIAID and intramuralscientists from the National Institute of Neurological Disorders andStroke (NINDS) indicate that T cells from patients with chronic Lymedisease are reactive not only against B. burgdorferi-specificantigens but also against various host (self) antigens (Nature Medicine5: 1375, 1999). Such antigenic mimicry might generate autoimmuneinflammatory reactions that could be responsible for arthritic as wellas some neurological symptoms associated with chronic Lyme disease.Intramural and extramural scientists are exploring the implications ofthis finding. $0$0Antibodies against the OspA epitopes of B. burgdorferi alsohave been shown to cross react with neural tissue (J. PeripheralNervousSystem 9, 165, 2004; J Neuroimmunol 159, 192, 2005) as well asmyocin (J Clin Microbiol 43, 850, 2005). Such antigenic mimicry mayhave the potential to generate autoimmune inflammatory reactions thatcould be responsible for the neurological symptoms associated withchronic Lyme disease. Intramural and extramural scientists areevaluating this possibility in greater detail. In this context, it isinteresting to note that homologies between proteins of B. burgdorferi and thyroid antigens also have been reported (Thyroid 14, 964, 2004). $0$0In clinical studies conducted by NIAID-supported extramuralscientists, case subject patients with post-treatment chronic Lymedisease (PTCLD) were compared to control subjects without such symptomsfor the presence of several human leukocyte antigen (HLA) class II(DRB1 and DQB1) genetic markers, some of which are known to beassociated with the expression of autoimmune reactivity. The resultsobtained did not support the involvement of an autoimmune mechanism inPTCLD (J Infect Dis :192, 1010, 2005) . However, since not allautoimmune diseases are associated with specific HLA haplotypes, thesefindings do not necessarily exclude that possibility. Definitive proofclearly would involve demonstrating the presence of significant levelsof relevant autoimmune antibodies and/or autoreactive T cells inpatients with PTCLD but not in treated control subjects without suchsymptoms. A greater frequency of DRB1*0401, which has been reported tobe associated with antibiotic-treatment resistant arthritis (Science281: 703, 1998) was noted in the case subject patients; although thisfinding appeared to be nominally significant (p < 0.05), itsbiological significance is ambiguous since none of the case subjectsconsidered had symptoms of inflammatory arthritis.$0$0$0$0in other words without the mumbo jumbo i am one sick ass dude.. $0$0$0$0$0$0