ArticleArthritis and rheumatism2009
HLA-DR alleles determine responsiveness to Borrelia burgdorferi antigens in a mouse model of self-perpetuating arthritis.
Article in Arthritis and rheumatism, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 39 citations in OpenAlex.
- Infection-Triggered Immune Dysregulation and Immunopathology in Lyme Disease: Mechanisms and Clinical Implications.Journal of clinical medicine · 2026Review
- Aspects of the Immunopathogenesis of Lyme Arthritis.Microorganisms · 2025Review
- Lyme Arthritis: A 50-Year Journey.The Journal of infectious diseases · 2024Article
- Genome-wide DNA Methylation Profiling in Lyme Neuroborreliosis Reveals Altered Methylation Patterns of HLA Genes.The Journal of infectious diseases · 2024Article
- A Review of Post-treatment Lyme Disease Syndrome and Chronic Lyme Disease for the Practicing Immunologist.Clinical reviews in allergy & immunology · 2022Review
- Lyme arthritis: linking infection, inflammation and autoimmunity.Nature reviews. Rheumatology · 2021Review
- Case Report: PANDAS and Persistent Lyme Disease With Neuropsychiatric Symptoms: Treatment, Resolution, and Recovery.Frontiers in psychiatry · 2021Article
- Posttreatment Lyme disease syndromes: distinct pathogenesis caused by maladaptive host responses.The Journal of clinical investigation · 2020Review
- Differences in clinicopathologic variables between Borrelia C6 antigen seroreactive and Borrelia C6 seronegative glomerulopathy in dogs.Journal of veterinary internal medicine · 2019Article
- Investigating disease severity in an animal model of concurrent babesiosis and Lyme disease.International journal for parasitology · 2019Review
- Evolutionary aspects of emerging Lyme disease in Canada.Applied and environmental microbiology · 2015Review
- Complex population structure of Borrelia burgdorferi in southeastern and south central Canada as revealed by phylogeographic analysis.Applied and environmental microbiology · 2015Article
- Natural killer cells and natural killer T cells in Lyme arthritis.Arthritis research & therapy · 2013Article
- Tick-specific borrelial antigens appear to be upregulated in American but not European patients with Lyme arthritis, a late manifestation of Lyme borreliosis.The Journal of infectious diseases · 2013Article
- Relationship between immunity to Borrelia burgdorferi outer-surface protein A (OspA) and Lyme arthritis.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2011Review
- Treg cell numbers and function in patients with antibiotic-refractory or antibiotic-responsive Lyme arthritis.Arthritis and rheumatism · 2010Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
objectiveArthritis is a prominent manifestation of Lyme disease, which is caused by infection with Borrelia burgdorferi (Bb). Chronic Lyme arthritis persisting even after antibiotic treatment is linked to HLA-DRB1*0401 (DR4) and related alleles. In contrast, patients whose Lyme arthritis resolves within 3 months postinfection show an increased frequency of HLA-DRB1*1101 (DR11). The aim of this study was to analyze the underlying mechanism by which HLA-DR alleles confer genetic susceptibility or resistance to antibiotic-refractory Lyme arthritis.
methodsWe generated DR11-transgenic (DR11-Tg) mice on a murine MHCII-/- background and compared their immune response to Bb antigens with the response of DR4-Tg mice after immunization with Bb outer surface protein A (OspA) or infection with live Bb.
resultsT cells from OspA-immunized and Bb-infected DR11-Tg mice had defective production of interferon-gamma as compared with those from DR4-Tg mice. In contrast, DR11-Tg mice developed higher titers of anti-OspA and anti-Bb antibodies, respectively, than did DR4-Tg mice. Consistent with this observation, we found that the Bb-infected DR11-Tg mice had a decreased spirochetal burden as compared with the DR4-Tg mice, as measured by quantitative polymerase chain reaction.
conclusionThis study provides direct evidence that in the presence of HLA-DR11, the immune response against Bb antigens is directed toward a protective antibody response. In contrast, an inflammatory Th1 response is induced in the presence of DR4. These observations offer an explanation for the differential genetic susceptibility of DR4+ and DR11+ individuals to the development of chronic Lyme arthritis and, eventually, the progression to antibiotic-refractory Lyme arthritis.
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