Table 1.
B. burgdorferi’s interface with mammalian hosts and its effect on Borrelia survival.
| Immune response modulators | Effects | Reference |
|---|---|---|
| Co-evolution of B. burgdorferi and its hosts | Host specialization and evolution of virulence- and infectivity-associated genes | (19, 20) |
| Tick salivary proteins | Suppression of pro-inflammatory responses in the host | (33, 34, 125) |
| Spirochete morphology and motility | Increase in B. burgdorferi dissemination and persistence | (38, 39) |
| B. burgdorferi adhesins | Interactions with host tissues, contributing to dissemination and persistence | (49, 50) |
| Host interactive proteins | Binding to host enzymes, such as plasmin/plasminogen; facilitates extracellular matrix degradation | (50, 52) |
| CRASPs | Decreased and inhibited complement activation | (60, 62, 63) |
| Modulation of protein expression | Adaptation to host, downregulation of immunogenic proteins, and antigenic variation | (79, 80) |
| Inappropriate macrophage activation | Extracellular matrix degradation | (54) |
| Antibodies with IgM-skewed isotype profile and of low affinity | Decreased antibody response quality which may contribute to persistence | (see text footnote) (73–75) |
| Loss of demarcated T and B cell zones in secondary lymphoid tissues and collapse of germinal centers | Reduced antibody class switch recombination and somatic affinity maturation. Failure to induce long-lived plasma cells and memory B cells in a timely manner | (69, 73, 74, 110) |