Borrelia burgdorferi-infected mice develop acute arthritis that underg
oes Ab-mediated resolution. To further investigate the role of B. burg
dorferi-specific Abs in Lyme borreliosis, CD40 ligand-deficient (CD40L
-deficient) mice were infected with B. burgdorferi. The development an
d regression of arthritis were similar in CD40L-deficient and control
mice. Although CD40L-deficient mice have defects in Ig class switching
, infected CD40L-deficient mice developed B. burgdorferi-specific IgG2
b Abs. Moreover, the transfer of serum from B. burgdorferi-infected CD
40L-deficient animals prevented infection in severe combined immunodef
icient mice. These data show that B. burgdorferi-infected CD40L-defici
ent mice are capable of producing Abs that are protective, despite the
inability of these mice to mediate T-dependent immune responses.