B-cell deficiency suppresses vaccine-induced protection against murine filariasis but does not increase the recovery rate for primary infection

To establish the role of B cells and antibodies in destroying filariae, mic e lacking mature B cells and therefore unable to produce antibodies were us ed. Litomosoides sigmodontis offers a good opportunity for this study becau se it is the only filarial species that completes its life cycle in mice. I ts development was compared in B-cell-deficient mice (BALB/c mu MT mice) an d wild-type BALB/c mice in two different in vivo situations, vaccination wi th irradiated larvae and primary infection. In all cases, mice were challen ged with subcutaneous inoculation of 40 infective larvae. Vaccine-induced p rotection was suppressed in B-cell-deficient mice. In these mice, eosinophi ls infiltrated the subcutaneous tissue normally during immunization; howeve r, their morphological state did not change following challenge inoculation , whereas in wild-type mice the percentage of degranulated eosinophils was markedly increased. From this, it may be deduced that the eosinophil-antibo dy-B-cell complex is the effector mechanism of protection in vaccinated mic e and that its action is fast and takes place in the subcutaneous tissue. I n primary infection, the filarial survival and growth was not modified by t he absence of B cells. However, no female worm had uterine microfilariae, n or did any mice develop a patent infection. In these mice, concentrations o f type 1 (gamma interferon) and type 2 (interleukin-4 [IL-4], IL-5 and IL-1 0) cytokines in serum were lower and pleural neutrophils were more numerous . The effects of the mu MT mutation therefore differ from those in B1-cell- deficient mice described on the same BALB/c. background, which reveal a hig her filarial recovery rate and microfilaremia. This outlines B2-cell-depend ent mechanisms as favorable to the late maturation of L. sigmodontis.