Borreliose / Lyme: the pathway in the body

Borreliose / Lyme is part of the pathway “Borrelia”. This page shows the whole pathway; the station of Borreliose / Lyme is highlighted.

Where this laboratory value sits: IgG antibodies — after class switching. Later, B cells switch to the IgG class with the help of the enzyme AID. IgG antibodies bind their target more tightly and remain detectable in the blood for a long time. Source 4, 5

In brief

Borrelia are spiral-shaped bacteria that ticks transmit while feeding on blood. In the body, immune cells recognise their surface proteins, and B cells form antibodies that can be detected in the blood.

The pathway step by step

1. Borrelia in the tick → Coat is remodelled Regulator RpoS · Blood meal As soon as the tick feeds on blood, temperature, acidity and nutrients in its gut change. Using their own regulator, the bacteria switch their surface proteins: OspA down, OspC up. Source 1, 2
2. Coat is remodelled → In the salivary gland With their new coat the bacteria detach from the gut wall, cross the tick's body cavity and reach its salivary gland. Depending on the tick species this takes one to two days. Source 2
3. In the salivary gland → In the skin · Salp15 and others The bacteria enter the skin with the saliva. Proteins from tick saliva, such as Salp15, bind to OspC and dampen the first response of immune cells there. Source 2, 1
4. In the skin → In connective tissue Adhesins DbpA/B · BBK32 Borrelia move through dense tissue in a corkscrew motion using internal flagella. Adhesins such as DbpA/B and BBK32 bind to decorin and fibronectin, building blocks of connective tissue. Source 3
5. Innate immunity → Antigen presentation Dendritic cells engulf fragments of the bacteria, migrate to the nearest lymph node and present the fragments to T cells there. Source 4, 5
6. Antigen presentation → B cells T helper cells B cells whose receptor matches a presented fragment multiply with the help of T helper cells and turn into cells that release antibodies. Source 5
7. B cells → IgM antibodies Antibodies of the IgM class appear first. They consist of five linked units and can bind several bacteria at once. Source 4
8. IgM antibodies → IgG antibodies Class switch (AID) Later, B cells switch to the IgG class with the help of the enzyme AID. IgG antibodies bind their target more tightly and remain detectable in the blood for a long time. Source 4, 5
9. IgG antibodies → Target structures bind to A short section of VlsE, called IR6, stays the same in every version. Antibodies against it, and against OspC or the flagellar protein p41, can be detected in the blood. Source 7, 6
10. Antigenic variation → Target structures A short section of VlsE, called IR6, stays the same in every version. Antibodies against it, and against OspC or the flagellar protein p41, can be detected in the blood. Source 7, 6

Cofactors in this pathway

• Zinc — Needed for signalling and proliferation of T and B cells; component of many zinc finger proteins Source 9In the ORY catalogue as a laboratory value: Zink
• Vitamin D — Calcitriol regulates genes in phagocytes, dendritic cells and lymphocytes via the vitamin D receptor Source 10In the ORY catalogue as a laboratory value: Vitamin D
• Iron — Needed for lymphocyte cell division and for the formation of oxygen radicals in phagocytes Source 12In the ORY catalogue as a laboratory value: Eisen
• Selenium — Component of selenoproteins such as the glutathione peroxidases in immune cells Source 11In the ORY catalogue as a laboratory value: Selen
• Manganese — Metal in enzymes and gene regulators of Borrelia; the bacteria manage without iron Source 8, 13

Sources

1. Radolf JD, Caimano MJ et al. Of ticks, mice and men: understanding the dual-host lifestyle of Lyme disease spirochaetes. Nat Rev Microbiol 2012 · PubMed 22230951
2. Kurokawa C, Lynn GE et al. Interactions between Borrelia burgdorferi and ticks. Nat Rev Microbiol 2020 · PubMed 32651470
3. Brissette CA, Gaultney RA. That's my story, and I'm sticking to it--an update on B. burgdorferi adhesins. Front Cell Infect Microbiol 2014 · PubMed 24772392
4. Petzke M, Schwartz I. Borrelia burgdorferi Pathogenesis and the Immune Response. Clin Lab Med 2015 · PubMed 26593255
5. Tracy KE, Baumgarth N. Borrelia burgdorferi Manipulates Innate and Adaptive Immunity to Establish Persistence in Rodent Reservoir Hosts. Front Immunol 2017 · PubMed 28265270
6. Norris SJ. vls Antigenic Variation Systems of Lyme Disease Borrelia: Eluding Host Immunity through both Random, Segmental Gene Conversion and Framework Heterogeneity. Microbiol Spectr 2014 · PubMed 26104445
7. Lawrenz MB, Hardham JM et al. Human antibody responses to VlsE antigenic variation protein of Borrelia burgdorferi. J Clin Microbiol 1999 · PubMed 10565921
8. Posey JE, Gherardini FC. Lack of a role for iron in the Lyme disease pathogen. Science 2000 · PubMed 10834845
9. Wessels I, Maywald M, Rink L. Zinc as a Gatekeeper of Immune Function. Nutrients 2017 · PubMed 29186856
10. Aranow C. Vitamin D and the immune system. J Investig Med 2011 · PubMed 21527855
11. Avery JC, Hoffmann PR. Selenium, Selenoproteins, and Immunity. Nutrients 2018 · PubMed 30200430
12. Nairz M, Weiss G. Iron in infection and immunity. Mol Aspects Med 2020 · PubMed 32461004
13. Troxell B, Yang XF. Metal-dependent gene regulation in the causative agent of Lyme disease. Front Cell Infect Microbiol 2013 · PubMed 24298449

Whole pathway: Borrelia

Related pathways

• Helicobacter pylori — igg antibodies
• IgG antibodies to food — antigen presentation
• 8-OHdG — Zink, Eisen
• Calprotectin — Zink, Eisen
• Cortisol — Zink, Eisen

As of 2026-09-16. Draft written by Claude to schema v2; sources checked in PubMed; expert review pending
Legal notice Privacy policy All biomarkers