Schistosoma mansoni: evidence that immunity in vaccinated and chronically infected CBA/Ca mice is sensitive to treatment with a monoclonal antibody that depletes cutaneous effector cells.

Naive mice, mice vaccinated 4 weeks previously with radiation-attenuated cercariae of Schistosoma mansoni and mice infected 16 weeks previously with normal S. mansoni cercariae were treated with a rat monoclonal antibody (NIMP-R14), that has been reported elsewhere to recognize neutrophils selectively. The establishment of a primary schistosome population in naive mice was not affected by the administration of this reagent. In contrast, immune-dependent challenge elimination was reduced in both vaccinated and chronically infected mice following treatment with NIMP-R14. Maximal suppression of resistance in both vaccinated (67% mean reduction) and chronically infected (44% mean reduction) mice was achieved when NIMP-R14 was injected intraperitoneally on the day of challenge. The monoclonal was markedly less effective when administered on or after day 3. Analysis of the blood leucocyte profiles of vaccinated/NIMP-R14 treated mice showed that the monoclonal totally abrogated neutrophils from the peripheral circulation between days 1 and 6. Histological examination of the skin site of challenge revealed, however, that NIMP-R14 treatment had reduced the number of eosinophils and macrophages as well as neutrophils in the cutaneous tissues of vaccinated mice. The reaction site thus more closely resembled that of naive/challenged mice than that of untreated vaccinated/challenged mice. Although we have not been able to identify a specific effector cell from these studies, we have demonstrated clearly that a skin-located cellular effector mechanism contributes to immune resistance in both murine models.