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 journalArticle

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
Externally publishedYes

Fingerprint

T-cells
Allergens
T-Lymphocytes
Interleukin-5
Eosinophilia
Time and Motion Studies
Interleukin-13
Adoptive Transfer
T-Lymphocyte Subsets
Time and motion study
Interleukin-4
Immunoglobulin E
Ablation
Lung

Keywords

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

ASJC Scopus subject areas

  • Cell Biology
  • Pulmonary and Respiratory Medicine
  • Molecular Biology

Cite this

Airway hyperresponsiveness in the absence of CD4+ T cells after primary but not secondary challenge. / Joetham, Anthony; Takeda, Katsuyuki; Taube, Christian; Miyahara, Nobuaki; Kanehiro, Arihiko; Dakhama, Azzeddine; Gelfand, Erwin W.

In: American Journal of Respiratory Cell and Molecular Biology, Vol. 33, No. 1, 07.2005, p. 89-96.

Research output: Contribution to journalArticle

Joetham, Anthony ; Takeda, Katsuyuki ; Taube, Christian ; Miyahara, Nobuaki ; Kanehiro, Arihiko ; Dakhama, Azzeddine ; Gelfand, Erwin W. / Airway hyperresponsiveness in the absence of CD4+ T cells after primary but not secondary challenge. In: American Journal of Respiratory Cell and Molecular Biology. 2005 ; Vol. 33, No. 1. pp. 89-96.
@article{e1c767c31a8a4de1a0e00ca002795949,
title = "Airway hyperresponsiveness in the absence of CD4+ T cells after primary but not secondary challenge",
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.",
keywords = "Airway hyperresponsiveness, CD4 T cells, Inflammation, Secondary challenge",
author = "Anthony Joetham and Katsuyuki Takeda and Christian Taube and Nobuaki Miyahara and Arihiko Kanehiro and Azzeddine Dakhama and Gelfand, {Erwin W.}",
year = "2005",
month = "7",
doi = "10.1165/rcmb.2004-0414OC",
language = "English",
volume = "33",
pages = "89--96",
journal = "American Journal of Respiratory Cell and Molecular Biology",
issn = "1044-1549",
publisher = "American Thoracic Society",
number = "1",

}

TY - JOUR

T1 - Airway hyperresponsiveness in the absence of CD4+ T cells after primary but not secondary challenge

AU - Joetham, Anthony

AU - Takeda, Katsuyuki

AU - Taube, Christian

AU - Miyahara, Nobuaki

AU - Kanehiro, Arihiko

AU - Dakhama, Azzeddine

AU - Gelfand, Erwin W.

PY - 2005/7

Y1 - 2005/7

N2 - 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.

AB - 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.

KW - Airway hyperresponsiveness

KW - CD4 T cells

KW - Inflammation

KW - Secondary challenge

UR - http://www.scopus.com/inward/record.url?scp=21844462859&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=21844462859&partnerID=8YFLogxK

U2 - 10.1165/rcmb.2004-0414OC

DO - 10.1165/rcmb.2004-0414OC

M3 - Article

VL - 33

SP - 89

EP - 96

JO - American Journal of Respiratory Cell and Molecular Biology

JF - American Journal of Respiratory Cell and Molecular Biology

SN - 1044-1549

IS - 1

ER -