ArticlePLoS pathogens2011
Lymphoadenopathy during lyme borreliosis is caused by spirochete migration-induced specific B cell activation.
Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 77 citations in OpenAlex.
- Borrelia burgdorferi disrupts gut barrier functions and microbiota-antibody interactions.The Journal of experimental medicine · 2026Article
- Mostly getting along -Borrelia burgdorferi and its manipulation of the host immune system.ImmunoHorizons · 2026Review
- Developing a durable, memory-driven, CspZ-targeting Lyme disease vaccine by rational adjuvant selection.NPJ vaccines · 2026Article
- Innate immune responses tomBio · 2026Article
- Testing the capacity of humanized immune system mice to induce a protective antibody response against the Lyme disease pathogen.Microbiology spectrum · 2026Article
- Develop a durable, memory-driven, CspZ-targeting Lyme disease vaccine by rationale adjuvant selection.bioRxiv : the preprint server for biology · 2026Article
- Characterizing the impact of intracutaneous dissemination on host responses duringFrontiers in immunology · 2026Article
- Polyvalent mRNA vaccine targeting outer surface protein C affords multi-strain protection against Lyme disease.NPJ vaccines · 2025Article
- Evaluation of Immune Response Dynamics: Analyzing the Parameters of Complete Blood Count (CBC) in Experimental Borreliosis.Life (Basel, Switzerland) · 2025Article
- Targeted volume imaging reveals early vascular interactions of Lyme disease pathogen in skin.Nature communications · 2025Article
- Article
- Novel recombinant vaccinia virus-vectored vaccine affords complete protection against homologousEmerging microbes & infections · 2024Article
- Bridging the gap: Insights in the immunopathology of Lyme borreliosis.European journal of immunology · 2024Review
- Mouse Models for the Study of Borrelia burgdorferi Infection.Current protocols · 2024Article
- Suppression of host humoral immunity byInfection and immunity · 2024Article
- Host glycosylation of immunoglobulins impairs the immune response to acute Lyme disease.EBioMedicine · 2024Article
- Borrelia burgdorferi Infection-Induced Persistent IgM Secretion Controls Bacteremia, but Not Bacterial Dissemination or Tissue Burden.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Antigen-Specific CD4 T Cell and B Cell Responses to Borrelia burgdorferi.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Choreography of Lyme Disease Spirochete Adhesins To Promote Vascular Escape.Microbiology spectrum · 2023Article
- Immune evasion strategies of major tick-transmitted bacterial pathogens.Trends in microbiology · 2023Review
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Authors and funding
6 authors at 1 institution in 1 country.
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Abstract
Lymphadenopathy is a hallmark of acute infection with Borrelia burgdorferi, a tick-borne spirochete and causative agent of Lyme borreliosis, but the underlying causes and the functional consequences of this lymph node enlargement have not been revealed. The present study demonstrates that extracellular, live spirochetes accumulate in the cortical areas of lymph nodes following infection of mice with either host-adapted, or tick-borne B. burgdorferi and that they, but not inactivated spirochetes, drive the lymphadenopathy. The ensuing lymph node response is characterized by strong, rapid extrafollicular B cell proliferation and differentiation to plasma cells, as assessed by immunohistochemistry, flow cytometry and ELISPOT analysis, while germinal center reactions were not consistently observed. The extrafollicular nature of this B cell response and its strongly IgM-skewed isotype profile bear the hallmarks of a T-independent response. The induced B cell response does appear, however, to be largely antigen-specific. Use of a cocktail of recombinant, in vivo-expressed B. burgdorferi-antigens revealed the robust induction of borrelia-specific antibody-secreting cells by ELISPOT. Furthermore, nearly a quarter of hybridomas generated from regional lymph nodes during acute infection showed reactivity against a small number of recombinant Borrelia-antigens. Finally, neither the quality nor the magnitude of the B cell responses was altered in mice lacking the Toll-like receptor adaptor molecule MyD88. Together, these findings suggest a novel evasion strategy for B. burgdorferi: subversion of the quality of a strongly induced, potentially protective borrelia-specific antibody response via B. burdorferi's accumulation in lymph nodes.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.