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Dragana Jankovic^*, Allen W. Cheever^*,, Marika C. Kullberg^*, Thomas A. Wynn^*, George Yap^*, Patricia Caspar^*, Fred A. Lewis, Raphael Clynes, Jeffrey V. Ravetch, and Alan Sher^*

From the ^* Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892; The Biomedical Research Institute, Rockville, Maryland 20852; and The Rockefeller University, 1230 York Avenue, New York, New York 10021

The effector functions of CD4⁺ T lymphocytes are generally thought to be controlled by distinct populations of regulatory T cells and their soluble products. The role of B cells in the regulation of CD4-dependent host responses is less well understood. Hepatic egg granuloma formation and fibrosis in murine schistosomiasis are dependent on CD4⁺ lymphocytes, and previous studies have implicated CD8⁺ T cells or cross-regulatory cytokines produced by T helper (Th) lymphocytes as controlling elements of this pathologic process. In this report, we demonstrate that B cell–deficient (µMT) mice exposed to Schistosoma mansoni develop augmented tissue pathology and, more importantly, fail to undergo the spontaneous downmodulation in disease normally observed during late stages of infection. Unexpectedly, B cell deficiency did not significantly alter T cell proliferative response or cause a shift in the Th1/Th2 balance. Since schistosome-infected Fc receptor–deficient (FcR chain knockout) mice display the same exacerbated egg pathology as that observed in infected µMT mice, the B cell– dependent regulatory mechanism revealed by these experiments appears to require receptor-mediated cell triggering. Together, the data demonstrate that humoral immune response/FcR interactions can play a major role in negatively controlling inflammatory disease induced by CD4⁺ T cells.

M.C. Kullberg was supported in part by a grant from the Swedish Medical Research Council.

Address correspondence to Dragana Jankovic, Immunobiology Section, Laboratory of Parasitic Diseases, NIAID, NIH, Building 4, Room 126, 9000 Rockville Pike, MD 20892-0425. Phone: 301-496-8218; Fax: 301-402-0890; E-mail: djankovic{at}atlas.niaid.nih.gov

¹ Abbreviations used in this paper: µMT, B cell-deficient mice; KO, knockout; SEA, soluble schistosome egg Ag; WT, wild-type.

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