Clin Infect Dis. 2011 Feb;52 Suppl 3:s259-65.
Relationship between immunity to Borrelia burgdorferi outer-surface protein
A (OspA) and Lyme arthritis.
Steere AC, Drouin EE, Glickstein LJ.
Center for Immunology and Inflammatory Diseases, Massachusetts General
Hospital, Harvard Medical School, Boston, USA.asteere@partners.org
Antibiotic-refractory Lyme arthritis may result from Borrelia
burgdorferi-induced autoimmunity in affected joints. Such patients usually
have certain HLA-DRB1 molecules that bind an epitope of B. burgdorferi
outer-surface protein A (OspA), and cellular and humoral immune responses
to
OspA are greater in patients with antibiotic-refractory arthritis than in
those with antibiotic-responsive arthritis. Recent work in a mouse model
suggests that, during B. burgdorferi infection, OspA in genetically
susceptible individuals stimulates a particularly strong T(H)1 response,
which may be one of several factors that can help set the stage for a
putative autoimmune response in affected joints. However, vaccination with
OspA did not induce arthritis in this mouse model, and case and control
comparisons in human vaccine trials did not show an increased frequency of
arthritis among OspA-vaccinated individuals.
Thus, a vaccine-induced immune response to OspA does not replicate the
sequence of events needed in the natural infection to induce
antibiotic-refractory Lyme arthritis.
Publication Types:
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=212
17173&retmode=ref&cmd=prlinks
PMID: 21217173 [PubMed - in process]
[Non-text portions of this message have been removed]
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