Vγ4+ T cells regulate airway hyperreactivity to methacholine in ovalbumin-sensitized and challenged mice

Youn Soo Hahn, Christian Taube, Niyun Jin, Katsuyuki Takeda, Jung Won Park, J. M. Wands, M. Kemal Aydintug, Christina L. Roark, Michael Lahn, Rebecca L. O'Brien, Erwin W. Gelfand, Willi K. Born

Research output: Contribution to journalArticle

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Abstract

The Vγ4+ pulmonary subset of γδ T cells regulates innate airway responsiveness in the absence of αβ T cells. We now have examined the same subset in a model of allergic airway disease, OVA-sensitized and challenged mice that exhibit Th2 responses, pulmonary inflammation, and airway hyperreactivity (AHR). In sensitized mice, Vγ4+ cells preferentially increased in number following airway challenge. Depletion of Vγ4+ cells before the challenge substantially increased AHR in these mice, but had no effect on airway responsiveness in normal, nonchallenged mice. Depletion of Vγ1 + cells had no effect on AHR, and depletion of all TCR-δ + cells was no more effective than depletion of Vγ4 + cells alone. Adoptively transferred pulmonary lymphocytes containing Vγ4+ cells inhibited AHR, but lost this ability when Vγ4+ cells were depleted, indicating that these cells actively suppress AHR. Eosinophilic infiltration of the lung and airways, or goblet cell hyperplasia, was not affected by depletion of Vγ4+ cells, although cytokine-producing αβ T cells in the lung increased. These findings establish Vγ4+ γδ T cells as negative regulators of AHR and show that their regulatory effect bypasses much of the allergic inflammatory response coincident with AHR.

Original languageEnglish
Pages (from-to)3170-3178
Number of pages9
JournalJournal of Immunology
Volume171
Issue number6
Publication statusPublished - 2003 Sep 15

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Methacholine Chloride
Ovalbumin
T-Lymphocytes
Lung
Goblet Cells
T-Lymphocyte Subsets
Hyperplasia
Pneumonia
Lymphocytes
Cytokines

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

Cite this

Hahn, Y. S., Taube, C., Jin, N., Takeda, K., Park, J. W., Wands, J. M., ... Born, W. K. (2003). Vγ4+ T cells regulate airway hyperreactivity to methacholine in ovalbumin-sensitized and challenged mice. Journal of Immunology, 171(6), 3170-3178.
Hahn, Youn Soo ; Taube, Christian ; Jin, Niyun ; Takeda, Katsuyuki ; Park, Jung Won ; Wands, J. M. ; Aydintug, M. Kemal ; Roark, Christina L. ; Lahn, Michael ; O'Brien, Rebecca L. ; Gelfand, Erwin W. ; Born, Willi K. / Vγ4+ T cells regulate airway hyperreactivity to methacholine in ovalbumin-sensitized and challenged mice. In: Journal of Immunology. 2003 ; Vol. 171, No. 6. pp. 3170-3178.
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abstract = "The Vγ4+ pulmonary subset of γδ T cells regulates innate airway responsiveness in the absence of αβ T cells. We now have examined the same subset in a model of allergic airway disease, OVA-sensitized and challenged mice that exhibit Th2 responses, pulmonary inflammation, and airway hyperreactivity (AHR). In sensitized mice, Vγ4+ cells preferentially increased in number following airway challenge. Depletion of Vγ4+ cells before the challenge substantially increased AHR in these mice, but had no effect on airway responsiveness in normal, nonchallenged mice. Depletion of Vγ1 + cells had no effect on AHR, and depletion of all TCR-δ + cells was no more effective than depletion of Vγ4 + cells alone. Adoptively transferred pulmonary lymphocytes containing Vγ4+ cells inhibited AHR, but lost this ability when Vγ4+ cells were depleted, indicating that these cells actively suppress AHR. Eosinophilic infiltration of the lung and airways, or goblet cell hyperplasia, was not affected by depletion of Vγ4+ cells, although cytokine-producing αβ T cells in the lung increased. These findings establish Vγ4+ γδ T cells as negative regulators of AHR and show that their regulatory effect bypasses much of the allergic inflammatory response coincident with AHR.",
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Hahn, YS, Taube, C, Jin, N, Takeda, K, Park, JW, Wands, JM, Aydintug, MK, Roark, CL, Lahn, M, O'Brien, RL, Gelfand, EW & Born, WK 2003, 'Vγ4+ T cells regulate airway hyperreactivity to methacholine in ovalbumin-sensitized and challenged mice', Journal of Immunology, vol. 171, no. 6, pp. 3170-3178.

Vγ4+ T cells regulate airway hyperreactivity to methacholine in ovalbumin-sensitized and challenged mice. / Hahn, Youn Soo; Taube, Christian; Jin, Niyun; Takeda, Katsuyuki; Park, Jung Won; Wands, J. M.; Aydintug, M. Kemal; Roark, Christina L.; Lahn, Michael; O'Brien, Rebecca L.; Gelfand, Erwin W.; Born, Willi K.

In: Journal of Immunology, Vol. 171, No. 6, 15.09.2003, p. 3170-3178.

Research output: Contribution to journalArticle

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T1 - Vγ4+ T cells regulate airway hyperreactivity to methacholine in ovalbumin-sensitized and challenged mice

AU - Hahn, Youn Soo

AU - Taube, Christian

AU - Jin, Niyun

AU - Takeda, Katsuyuki

AU - Park, Jung Won

AU - Wands, J. M.

AU - Aydintug, M. Kemal

AU - Roark, Christina L.

AU - Lahn, Michael

AU - O'Brien, Rebecca L.

AU - Gelfand, Erwin W.

AU - Born, Willi K.

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N2 - The Vγ4+ pulmonary subset of γδ T cells regulates innate airway responsiveness in the absence of αβ T cells. We now have examined the same subset in a model of allergic airway disease, OVA-sensitized and challenged mice that exhibit Th2 responses, pulmonary inflammation, and airway hyperreactivity (AHR). In sensitized mice, Vγ4+ cells preferentially increased in number following airway challenge. Depletion of Vγ4+ cells before the challenge substantially increased AHR in these mice, but had no effect on airway responsiveness in normal, nonchallenged mice. Depletion of Vγ1 + cells had no effect on AHR, and depletion of all TCR-δ + cells was no more effective than depletion of Vγ4 + cells alone. Adoptively transferred pulmonary lymphocytes containing Vγ4+ cells inhibited AHR, but lost this ability when Vγ4+ cells were depleted, indicating that these cells actively suppress AHR. Eosinophilic infiltration of the lung and airways, or goblet cell hyperplasia, was not affected by depletion of Vγ4+ cells, although cytokine-producing αβ T cells in the lung increased. These findings establish Vγ4+ γδ T cells as negative regulators of AHR and show that their regulatory effect bypasses much of the allergic inflammatory response coincident with AHR.

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