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J. Exp. Med.,
Volume 187, Number 4, February 16, 1998 619-629
By
From the * Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and
Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892; 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 The Biomedical
Research Institute, Rockville, Maryland 20852; and § The Rockefeller University, 1230 York Avenue,
New York, New York 10021
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.
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