Ectopic expression of IL-5 identifies an additional CD4+ T cell mechanism of airway eosinophil recruitment

Jeffrey R. Crosby, H. H. Shen, M. T. Borchers, J. P. Justice, T. Ansay, J. J. Lee, N. A. Lee

Research output: Contribution to journalArticlepeer-review

16 Scopus citations


CD4+ T cells have a critical role in the development of allergic pulmonary inflammation, including the recruitment of eosinophils to the air-way lumen and interstitium. The expression of interleukin (IL)-5 by CD4+ cells has, in particular, often been lionized as the central link between allergic inflammation and the concomitant expansion or recruitment of eosinophils. The mechanism(s) by which CD4+ T cells mediates eosinophil recruitment was assessed with gene knockout mice deficient for T cells or T cell subtypes and a unique IL-5 transgenic mouse (line NJ. 1726) that constitutively overexpresses this cytokine in the lung epithelium. Pulmonary IL-5 expression is significantly attenuated in T cell- and CD4+ but not CD8+ cell-deficient animals, suggesting an obvious explanation for the lack of eosinophils in the lungs of T cell-deficient and CD4(-/-) mice. However, although the constitutive expression of IL-5 in the lung epithelium of NJ.1726 mice elicited an eosinophilia in the airway lumen of both naive and ovalbu-rain-treated mice, in the absence of CD4+ cells, allergen-mediated eosinophil recruitment to the bronchoalveolar lavage fluid was abolished. Moreover, intranasal instillation of the potent eosinophil-specific chemokine eotaxin-2 was incapable of eliciting eosinophil recruitment in naive and ovalbumin-treated NJ.1726 CD4(-/-) mice, suggesting that eosin-ophil trafficking during allergic inflammatory responses is a consequence of a CD4+ cell-mediated event(s) in addition to IL-5 expression and the establishment of a pulmonary chemokine gradient.

Original languageEnglish (US)
Pages (from-to)L99-L108
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number1 26-1
StatePublished - 2002


  • Allergy
  • Asthma
  • Gene knockout
  • Interleukin-5
  • Mouse model
  • Transgenic

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology


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