In the mouse model of
Lyme borreliosis, the host immune response during
infection with Borrelia burgdorferi results in the remission of
carditis and
arthritis, as well as global reduction of spirochete numbers in tissues, without elimination of
infection. These events were recapitulated by passive transfer of immune serum from infected immunocompetent mice or T-cell-deficient mice to severe combined immunodeficient (SCID) mice. Previous studies have shown that immune serum is reactive against
arthritis-related
protein (Arp) and that Arp antiserum induces
arthritis remission. However, although immune serum from T-cell-deficient mice induced disease remission, it was not reactive against Arp, suggesting that antibody to another
antigen may be responsible. T-cell-deficient mouse immune serum was reactive to
decorin binding protein A (
DbpA). Therefore,
DbpA antiserum was tested to determine its ability to induce disease remission in SCID mice.
Antisera to Arp or
DbpA induced both
carditis and
arthritis remission but did not significantly reduce spirochete numbers in tissues, based upon quantitative flaB
DNA analysis, nor did treatment affect
RNA levels of several genes, including arp and
dbpA. Immunohistochemical labeling of spirochetes in hearts and joints during disease remission induced by adoptive transfer of lymphocytes, passive transfer of immune serum, or passive transfer of
DbpA antiserum revealed that such treatment resulted in elimination of spirochetes from heart base and synovium but not vascular walls, tendons, or ligaments. These results suggest that Arp and
DbpA antibodies may be active as disease-resolving components in immune serum but antibody against other
antigens may be involved in reductions of spirochetes in tissues.