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Infection and Immunity, June 2003, p. 3097-3106, Vol. 71, No. 6
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.6.3097-3106.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

T Cells Are Required for Host Protection against Brugia malayi but Need Not Produce or Respond to Interleukin-4

Department of Pathology, University of Connecticut Health Center, Farmington, Connecticut 06030,¹ Jackson Laboratories, Bar Harbor, Maine 04609²

Received 26 November 2002/ Returned for modification 24 January 2003/ Accepted 6 March 2003

T cells are known to be required for host protection in mouse models of Brugia malayi infection. Several independent studies in murine models have also highlighted the rapid induction of Th2-like responses after infection with B. malayi or B. pahangi. Previous data from our laboratory have described a significant increase in permissiveness in the absence of interleukin-4 (IL-4), the "prototypical" Th2 cytokine, involved in both the induction and maintenance of Th2 responses. These observations led to our hypothesis that T cells involved in murine host protection would respond to IL-4 signaling and differentiate into cells of the "type 2" phenotype. As such, these cells would presumably also act as major sources of IL-4. To investigate these hypotheses, we performed several adoptive transfers in which we controlled the cell population(s) able to produce or respond to IL-4. We show here that, in contrast to our original hypotheses, IL-4 production and IL-4 receptor expression by T cells are both dispensable for T-cell-mediated host protection. Instead, our data imply that T cells may be required for eosinophil accumulation at the site of infection.

Editor: W. A. Petri, Jr.

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