Anti-lysoganglioside and other anti-neuronal autoantibodies in post-treatment Lyme Disease and Erythema Migrans after repeat infection.
Level 4 - case-series / case-control
Case-control observational study comparing autoantibody levels and cellular signaling across patient groups and controls
PubMed 34589824 · doi:10.1016/j.bbih.2019.100015
What was done
Serum antineuronal IgG titers against lysoganglioside GM1, tubulin, and dopamine receptors (D1R and D2R) were measured via ELISA across 179 participants: 24 with recent Erythema Migrans (EM) without prior Lyme disease (LD), 8 with recent EM and prior LD, 119 with persistent post-treatment LD symptoms (PTLS), and 28 seronegative endemic controls. Serum antibody-mediated signaling of calcium calmodulin-dependent protein kinase II (CaMKII) activity was also measured in a human neuronal cell line (SK-N-SH).
What was found
The EM with prior LD group (n = 8) showed significantly higher titers than controls for anti-lysoganglioside GM1 (p = 0.002), anti-tubulin (p = 0.03), and anti-D1R (p = 0.02), as well as increased antibody-mediated CaMKII signaling (p = 0.03). The PTLS group (n = 119) showed significantly higher anti-lysoganglioside GM1 titers than controls (p = 0.01) but not for the other markers. The primary EM group without prior LD (n = 24) showed no significant differences compared to controls. Absolute titer values were not reported in the abstract.
Why it matters
The findings suggest that repeat Borrelia burgdorferi exposure may induce an immune priming effect that elevates antineuronal antibodies with functional signaling activity, and that anti-lysoganglioside antibodies may play a role in persistent post-treatment symptoms.
Limits
The repeat EM subgroup was very small (n = 8), limiting statistical power. The study is cross-sectional and cannot establish whether autoantibodies cause symptoms or are incidental post-infectious markers. Absolute concentrations and clinical symptom correlations were not reported in the abstract.
Cited by
- context Lyme infection induces molecular mimicry via flagella, causing autoantibodies against dopamine receptors, thyroid tissue, cardiolipin, and myelin.