Airway hyperresponsiveness in the absence of CD4+ T cells after primary but not secondary challenge

Anthony Joetham, Katsuyuki Takeda, Christian Taube, Nobuaki Miyahara, Arihiko Kanehiro, Azzeddine Dakhama, Erwin W. Gelfand

Research output: Contribution to journalArticlepeer-review

11 Citations (Scopus)

Abstract

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 after either primary or secondary airway allergen challenge. After sensitization, CD4-deficiency in mice was not associated with airway eosinophilia, allergen-specific IgE, or elevated levels of interleukin (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 after 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 after 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 the cellular pathway, which may contribute to the development of AHR after primary allergen exposure of sensitized mice.

Original languageEnglish
Pages (from-to)89-96
Number of pages8
JournalAmerican journal of respiratory cell and molecular biology
Volume33
Issue number1
DOIs
Publication statusPublished - Jul 2005

Keywords

  • Airway hyperresponsiveness
  • CD4 T cells
  • Inflammation
  • Secondary challenge

ASJC Scopus subject areas

  • Molecular Biology
  • Pulmonary and Respiratory Medicine
  • Clinical Biochemistry
  • Cell Biology

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