T cells are required for host protection against Brugia malayi but need not produce or respond to interleukin-4.

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Eosinophils, Filariasis, Interleukin-13, Interleukin-4, Mice, Mice-Inbred-BALB-C, Mice-SCID, Receptors-Interleukin-4, SUPPORT-U-S-GOVT-P-H-S, T-Lymphocytes, Trans-Activators

JAX Source

Infect Immun 2003 Jun; 71(6):3097-3106.


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.