Protection against Borrelia burgdorferi infection in SCID mice is conferred by presensitized spleen cells and partially by B but not T cells alone.

Abstract

Borrelia burgdorferi induces spirochetemia, arthritis, carditis and myositis in SCID mice but not in immunocompetent co-isogenic C.B-17 mice. The contribution of naive or presensitized B and T cells in the control of spirochetal infection has now been analysed in SCID mice reconstituted with unselected spleen cells or enriched B or T cell populations thereof and subsequently challenged with B. burgdorferi. It is shown that SCID mice were protected (i) completely against disease (arthritis, carditis, myositis) by unselected spleen cells previously sensitized either to intact spirochetes or to recombinant outer surface protein A (OspA), (ii) to a large extent by mixtures of enriched spirochete-specific B and T cells, (iii) partially by equivalent preparations of presensitized B cells or by naive spleen or B cells, and (iv) not at all by presensitized or naive T cells alone. The degree of protection transferred was similar for the corresponding lymphocyte populations presensitized either to viable spirochetes or to recombinant OspA and correlated mainly with serum levels of B. burgdorferi-specific antibodies, in particular those to OspA/OspB. The capacity of enriched presensitized or naive B cells alone to generate specific antibodies of the isotypes IgM, IgG2b and IgG3, and to confer partial protection to SCID mice upon challenge with B. burgdorferi is most probably due to a B cell mitogen(s) associated with the spirochetes. These data further emphasize the important role of B cells and antibodies in the control of B. burgdorferi infection in mice, and suggest that T cells are critically involved in the optimal generation of protective antibody responses but not in the direct elimination of spirochetes from the host.