Dr. Jeffrey GladdenFounder & CEO of Gladden Longevity

The Role of Antibodies 🦠🦠

1 Jun 2026 · 2 min

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1:35

In this lecture Dr. Jeffrey Gladden explains how Borrelia spirochetes, after entering through the skin, impair the skin’s immune response by disrupting B‑cell follicle function and weakening germinal centers. This leads to either delayed antibody production or a hyper‑IgM profile where patients produce large amounts of low‑specificity IgM antibodies. The excess IgM drives helper T‑cell 2 (Th2) cytokine production (IL‑4, IL‑6), shifting the immune response away from protective Th1 cytokines such as interferon‑γ and IL‑12. The resulting inflammatory environment promotes further damaging feedback loops, including the production of type I interferons, which exacerbate tissue injury. The talk highlights the mechanistic cascade from spirochete entry to dysregulated humoral immunity and inflammation.

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So the— with the immune response, one of the first things that happen— think about pathogen defense, okay? So when the spirochetes are transmitted, the cells in the skin are defective in their ability to respond. So right out of the gate, the spirochete gets in, it's in the skin, it gets into the circulation, it goes to the tissues, and the body says, "Okay, I see it," and it tries to make antibodies. The Borrelia interfere with the follicles of the B cell. And so the germinal centers are weakened. And so right out of the gate, the antibodies that are produced are either fewer or there's a lot of them but their specificity and stringency aren't as good. And that's why patients are either delayed in making antibodies, some patients never make antibodies, but other patients have this hyper-IgM signature where all they're making are IgM antibodies and they're making a ton of them. And then that creates a destructive loop because you've got— IgM antibodies in the periphery, so now all the T cells that talk to the B cells are gonna produce what are called helper T cell 2 type cytokines. And those cytokines drive inflammation. And so you're skewing the immune system away from cytokines that can be deemed protective, things that people have heard of like interferon gamma, IL-12, and now you've got IL-4, IL-6. You've got, you know, chemokines and cytokines that are telling the immune system, you know, react with inflammation and in certain tissue sites that can cause production of other things that are feedback amplified and damaging like type 1 interferons.