| Molecular mimicry in Lyme arthritis demonstrated at the single cell level: LFA-1 alpha L is a partial agonist for outer surface protein A-reactive T cells. | |
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MedLine Citation:
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PMID: 11290815 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Antibiotic treatment-resistant Lyme arthritis is a chronic inflammatory joint disease that follows infection with Borrelia burgdorferi (BB:). A marked Ab and T cell response to BB: outer surface protein A (OspA) often develops during prolonged episodes of arthritis. Furthermore, cross-reaction between the bacterial OspA and human LFA-1alpha(L) at the T cell level and the inability to detect BB: in the joint implicate an autoimmune mechanism. To analyze the nature of response to OspA and LFA-1alpha(L), we used OspA-specific T cell hybrids from DR4 transgenic mice, as well as cloned human cells specific for OspA(165-184), the immunodominant epitope, from five DRB1*0401(+) patients, using OspA-MHC class II tetramers. Although OspA(165-184) stimulated nearly all OspA-specific human T cell clones tested to proliferate and secrete IFN-gamma and IL-13, LFA-1alpha(L326-345) stimulated approximately 10% of these clones to proliferate and a greater percentage to secrete IL-13. Assays with LFA- or OspA-DR4 monomers revealed that higher concentrations of LFA-DR4 were needed to stimulate dual-reactive T cell hybrids. Our analysis at the clonal level demonstrates that human LFA-1alpha(L326-345) behaves as a partial agonist, perhaps playing a role in perpetuating symptoms of arthritis. |
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Authors:
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C Trollmo; A L Meyer; A C Steere; D A Hafler; B T Huber |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Journal of immunology (Baltimore, Md. : 1950) Volume: 166 ISSN: 0022-1767 ISO Abbreviation: J. Immunol. Publication Date: 2001 Apr |
Date Detail:
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Created Date: 2001-04-06 Completed Date: 2001-06-28 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 2985117R Medline TA: J Immunol Country: United States |
Other Details:
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Languages: eng Pagination: 5286-91 Citation Subset: AIM; IM |
Affiliation:
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Laboratory of Molecular Immunology, Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antigens, Surface / immunology*, metabolism Bacterial Outer Membrane Proteins / agonists, immunology*, metabolism Bacterial Vaccines Borrelia burgdorferi Group / immunology* Clone Cells Humans Hybridomas Lipoproteins* Lyme Disease / immunology* Lyme Disease Vaccines / agonists, immunology*, metabolism Lymphocyte Activation / immunology* Lymphocyte Function-Associated Antigen-1 / immunology*, metabolism Mice Mice, Transgenic Molecular Mimicry* Peptide Fragments / agonists, immunology, metabolism T-Lymphocyte Subsets / immunology*, microbiology |
| Grant Support | |
ID/Acronym/Agency:
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AI39671/AI/NIAID NIH HHS; AR-07570/AR/NIAMS NIH HHS; AR-08541/AR/NIAMS NIH HHS; AR-20358/AR/NIAMS NIH HHS; AR-45386/AR/NIAMS NIH HHS; NS2424710/NS/NINDS NIH HHS; NS38037/NS/NINDS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Antigens, Surface; 0/Bacterial Outer Membrane Proteins; 0/Bacterial Vaccines; 0/Lipoproteins; 0/Lyme Disease Vaccines; 0/Lymphocyte Function-Associated Antigen-1; 0/OspA protein; 0/Peptide Fragments |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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