The granulomatous response in murine Schistosomiasis mansoni does not switch to Th1 in IL-4-deficient C57BL/6 mice.

Important note: Information in this article was accurate in 1997. The state of the art may have changed since the publication date.

The granulomatous response in murine Schistosomiasis mansoni does not switch to Th1 in IL-4-deficient C57BL/6 mice.

J Immunol. 1996 Nov 15;157(10):4546-53. Unique Identifier : AIDSLINE MED/97064214
Metwali A; Elliott D; Blum AM; Li J; Sandor M; Lynch R; Noben-Trauth N; Weinstock JV; Department of Internal Medicine, University of Iowa, Iowa City; 52242, USA.

Abstract: IL-4 plays an important role in polarizing inflammation toward a Th2 response. It remains uncertain, however, whether IL-4 also serves to prevent expression of Th1 inflammation. Therefore, using a genetically pure C57BL/6 IL-4-deficient mouse, we studied the role of IL-4 in regulating the production of IFN-gamma and Th1 inflammation in the granulomas of mice infected with Schistosoma mansoni. In contrast to normal animals, IL-4 mutant mice generated smaller liver granulomas that contained fewer eosinophils and no mast cells. Collagenase-dispersed granuloma cells were analyzed by flow cytometry and cultured in vitro to measure cytokine and Ig production. Compared with control granuloma cells, IL-4-/- cells secreted only small quantities of IL-5 and IL-10. Also, there was impaired expression of the IL-4-dependent molecules IgE and IgG1 as well as B cell surface class II and CD23. Yet the granulomas of IL-4 -/- animals produced little IFN-gamma, IgG2a, or other molecules associated with Th1 inflammation even after Ag or anti-CD3 stimulation. Splenocytes from IL-4 -/- animals stimulated with schistosome Ag also failed to produce a Th1 response. Our data show that most aspects of the Th2 response in murine schistosomiasis are highly dependent on IL-4 production. But in the absence of IL-4, neither the natural local granulomatous response to schistosome ova nor the systemic response to soluble egg Ag switches to the type 1 phenotype. Thus the production of IL-4 early in the inflammatory response is not the only factor preventing Th1 expression in inflammation.

Keywords: Animal B-Lymphocytes/IMMUNOLOGY Granuloma/GENETICS/*IMMUNOLOGY/*PATHOLOGY Interleukin-4/*DEFICIENCY Mice Mice, Inbred C57BL Mice, Knockout Schistosoma mansoni/IMMUNOLOGY Schistosomiasis mansoni/GENETICS/*IMMUNOLOGY/*PATHOLOGY Support, U.S. Gov't, Non-P.H.S. Support, U.S. Gov't, P.H.S. Th1 Cells/*IMMUNOLOGY JOURNAL ARTICLE
970228
M9721859

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