Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2011-1-10
pubmed:abstractText
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1537-6591
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
52 Suppl 3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
s259-65
pubmed:dateRevised
2011-6-3
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Relationship between immunity to Borrelia burgdorferi outer-surface protein A (OspA) and Lyme arthritis.
pubmed:affiliation
Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Harvard Medical School, Boston, USA. asteere@partners.org
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural