Published ahead of print on April 21, 2005, doi:10.1165/rcmb.2004-0414OC Am. J. Respir. Cell Mol. Biol., Volume 33, Number 1, July 2005, 89-96 A more recent version of this article appeared on July 1, 2005
Submitted on December 23, 2004 Airway Hyperresponsiveness in the Absence of CD4+ T Cells After Primary but not Secondary ChallengeAnthony Joetham1,1 Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO, USA * To whom correspondence should be addressed. E-mail: gelfande{at}njc.org.
CD4+ T cells have been shown to play a role in the development of airway hyperresponsivness (AHR) and airway eosinophilia in mice using ablation as well as adoptive transfer experiments. However, as other T cell subsets (CD8, NKT) may play a role in these models, we examined the responses of sensitized CD4-deficient mice following either primary or secondary airway allergen challenge. Following sensitization, CD4-deficient mice was not associated with airway eosinophilia, allergen-specific IgE or elevated levels of IL-4 or IL-13. Increases in lung CD8 T cells and IL-5 were observed and shown to be essential for AHR as demonstrated following CD8 T-cell depletion or anti-IL-5 treatment. In contrast to the response of sensitized CD4-deficient mice to primary allergen challenge, they failed to develop AHR following secondary allergen challenge. Although the importance of this CD4+ T-cell-independent pathway in normal mice is unclear at this time, these studies identify the diversity of cellular pathway which may contribute to the development of AHR following primary allergen exposure of sensitized mice.
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