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Lymphoadenopathy during Lyme Borreliosis Is Caused by Spirochete Migration-Induced Specific B Cell Activation

Posted By: CrystalRiver
Date: Wednesday, 13-Jan-2021 05:52:07
www.rumormill.news/128632

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3102705/

Lymphoadenopathy during Lyme Borreliosis Is Caused by Spirochete Migration-Induced Specific B Cell Activation
Stefan S. Tunev, 1 , 2 , ¤ Christine J. Hastey, 1 , 4 Emir Hodzic, 1 Sunlian Feng, 1 Stephen W. Barthold, 1 , 2 , 3 , 4 and Nicole Baumgarth 1 , 2 , 3 , 4 , *
Jenifer Coburn, Editor
Author information Article notes Copyright and License information Disclaimer
This article has been cited by other articles in PMC.
Associated Data
Supplementary Materials
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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.

Go to:
Author Summary
Acute Lyme Disease is one of the most important emerging diseases in the US. People with acute Lyme disease often develop swollen lymph nodes, or lymphadenopathy, but we do not know why this happens or what effect it has on the course of the disease. We show here that when mice are infected with live Borrelia burgdorferi spirochetes (the bacteria that cause Lyme disease), live spirochetes collect in the lymph nodes. These lymph nodes then swell up and start producing large numbers of antibody-producing cells. Although many of these antibodies can recognize the bacteria, they apparently lack the quality to clear the infection. We hypothesize that by moving into the lymph node, usually a site in which strong immune responses are induced, Borrelia evades the immune response: it goes to the lymph nodes and tricks the immune system into making a very strong but inadequate response.

Go to:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3102705/

-------------------------------------
Dear RM Agents and Readers,

Just in case you are experiencing this symptom as am I; I've recently put it together, hopefully this helps some of you as well. You might want to look at a diagram of the lymph system in order to verify what you may be experiencing and if the location correlates with the lymph system.

Many Blessings,
CrystalRiver



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AN EXPLANATION OF THE FACTIONS