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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

L. Spencer,1 L. Shultz,2 and T. V. Rajan1*

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.

* Corresponding author. Mailing address: Department of Pathology, University of Connecticut Health Center, 263 Farmington Ave., Farmington, CT 06030-3105. Phone: (860) 679-3221. Fax: (860) 679-2936. E-mail: rajan{at}neuron.uchc.edu.

Editor: W. A. Petri, Jr.

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.



This article has been cited by other articles:

  • Voehringer, D., Reese, T. A., Huang, X., Shinkai, K., Locksley, R. M. (2006). Type 2 immunity is controlled by IL-4/IL-13 expression in hematopoietic non-eosinophil cells of the innate immune system. JEM 203: 1435-1446 [Abstract] [Full Text]  
  • Rajan, B., Ramalingam, T., Rajan, T. V. (2005). Critical Role for IgM in Host Protection in Experimental Filarial Infection. J. Immunol. 175: 1827-1833 [Abstract] [Full Text]  


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