Within days to weeks after the initial infection, B. burgdorferi begins to move away from the site of infection to other areas of the body via blood and lymph. Plasma cells have been found in all areas infected by B. burgdorferi, and the humoral immune response produces antibodies to more than 10 polypeptides of B. burgdorferi (Fung et. al., 1994). The outer surface proteins (Osp) are recognized less often and later than expected in the humoral immune response.  Antibodies against OspA are not recognized until very late in the infection, if at all.  In addition, skin and CSF cultures from Lyme disease patients demonstrate low reactivity with anti-OspA antibodies (Pachner et. al., 1992).  OspA antibodies are more likely to be found in patients with chronic infection (Benach et. al., 1988).  Based on the surface location and abundance of OspA in B. burgdorferi, it is puzzling that antibodies against OspA are not produced earlier and in greater abundance. Various hypotheses have been presented to account for this interesting phenomenon. The bacterium may undergo antigenic shift leading to the delay of the expression of this protein, thereby delaying the host’s immune recognition. Another possibility is that OspA is simply weekly immunogenic in humans (Benach et. al., 1988).   

Despite the early weak immunogenicity of OspA, OspA is an important antibody in patients with chronic, severe Lyme arthritis. An early study showed that patients with Lyme arthritis showed a strong IgG response to both OspA and OspB during early stages of chronic arthritis.  A subsequent study found a very low antibody response to OspA and OspB, which correlates with the down-regulation of these Osps after transmission into the human host.  (Akin et. al, 1999). However, patients with severe, chronic arthritis demonstrated increased antibody response to OspA and OspB later in infection. Akin et. al further demonstrated that early in illness, IgM antibodies were produced in response to OspC and OspF, which makes sense in light of the up-regulation of OspC upon spirochetal entry into the human host (see Structural Features).  Furthermore, IgG antibody response to OspC was only seen in patients with prolonged arthritis, while the IgM response to OspC were high during early infection (Akin et. al.) 

Antibodies are more commonly produced against flagellar proteins (Szczepanski and Benach, 1991).  The humoral immune response involves production of IgM, IgG, and less often IgE antibodies. The initial specific B-cell response involves IgM antibodies, and specific IgM antibodies are produced in response to the 41-kd flagellar antigen of the bacterium (Steere, 1989).  IgM antibodies are usually produced 3-6 weeks after infection (Szczepanski and Benach, 1991).  IgG antibodies are usually detected six weeks after infection.  The IgG antibody response develops in reaction to various bacterial peptides, including:  31 – 34 and 66-kd outer surface proteins, the 41-kd flagellar antigen, and the 55/58-kd antigen (Steere, 1989).  Antibodies of the IgG1 and IgG3 subclasses are most commonly produced, while IgG2 is produced in response to carbohydrate and lipopolysaccharide. Carbohydrates of B. burgdorferi are not strong immunogens, demonstrated by the low level of IgG2 in most patients (Hechemy et. al., 1988).  

Antibodies neutralize and opsonize the bacterium, allowing activation of the classical complement pathway as well as phagocytosis by PMNs and monocytes (Steere, 1989).  Overall, evidence of the humoral immune response is provided by the presence of circulating immune factors including specific antibodies, immune complexes, and cyroglobulins (Szczepanski and Benach, 1991).

This page was created for an undergraduate Immunology course, Biology 307, at Davidson College in the Spring semester of 2007 under Dr. Sophia Sarafova (sasarafova@davidson.edu)

Please direct all comments and questions to Meredith Prasse (meprasse@davidson.edu)