The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1998/2/619/ $5.00
The Journal of Experimental Medicine, Volume 187, Number 4, February 16, 1998 619-629

Articles

CD4+ T Cell–mediated Granulomatous Pathology in Schistosomiasis Is Downregulated by a B Cell–dependent Mechanism Requiring Fc Receptor Signaling

Dragana Jankovic*, Allen W. Cheever*,{ddagger}, Marika C. Kullberg*, Thomas A. Wynn*, George Yap*, Patricia Caspar*, Fred A. Lewis{ddagger}, 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; {ddagger} 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 {gamma} 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.

We thank Drs. S.L. James and T. Nutman for reading the manuscript, and R. Dryfuss and S. Everett for help with the photomicrographs.

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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