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Is it thee or me?—autoimmunity in Lyme disease
Mark S. Klempner & Brigitte T. Huber

Nature Medicine 5, 1346 - 1346-1347 (1999)



Figure 1: Molecular mimicry in chronic Lyme Disease.

Within weeks after Borrelia burgdorferi (Spirochete – yellow cell) infection, patients develop acute phase symptoms such as skin rash, meningitis, neuritis, encephalitis, myocarditis, and flu-like symptoms. The infection is frequently resolved by the immune response or antibiotic treatment. The immune response involves

  1. Borrelia burgdorferi uptake by antigen presenting cells (APC – purple star-shaped cells),
  2. proteolytic processing of the Borrelia burgdorferi proteins Osp A (hexagon), Osp C (triangle, ), p37 (circle, ) and p22 (square, ), and
  3. presentation of peptides derived from these proteins to T cells (blue circular cells).
  4. T cells that recognize these epitopes, presented by APC in the context of MHC, proliferate.
Absence of antibiotic treatment or failure of the immune response leads to spirochete persistence which causes acrodermatitis, arthritis or neurologic symptoms.
Despite appropriate antibitotic treatment, some patients develop treatment-resistant arthritis, encephalopathy or radiculopathy.

Autoimmunity may cause these symptoms

  • since T cells that recognize Borrelia burgdorferi processed peptide OspA are also capable of attacking LFA1, leading to joint tissue damage.
  • In the central nervous system. T cells that react to
    • OspA,
    • OspC, and
    • p22
    epitopes also recognize
    • MOBP,
    • SST-R1, and
    • IL-1R,
    respectively, on neurons, possibly leading to encephalopathy and radiculopathy.
T cell recognition of synovial and neuronal proteins can cause chronic symptoms for years after the initial infection. It is not known
  • whether the spirochete is still present during this chronic stage, or
  • whether the symptoms are strictly due to T cell autoimmunity.

Copyright 1999 Nature America Inc.