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Negative regulation of airway responsiveness that is dependent on γδ T cells and independent of αβ T cells

An Erratum to this article was published on 01 February 2000

Abstract

The mechanisms regulating airway function are complex and still poorly understood. In diseases such as asthma, involvement of immune-dependent mechanisms has been suggested in causing changes in airway responsiveness to bronchoconstrictors. We now demonstrate that γδ T cells can regulate airway function in an αβ T cell-independent manner, identifying them as important cells in pulmonary homeostasis. This function of γδ T cells differs from previously described immune-dependent mechanisms and may reflect their interaction with innate systems of host defense.

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Figure 1: AHR and BAL fluid cells in mice deficient of γδ or αβ T cells after systemic sensitization and airway challenge with OVA (2ip3N protocol).
Figure 2: Lung tissue of C57BL/6, TCR-δ–/– and TCR-β–/– mice after systemic sensitization and airway challenge with OVA (2ip3N) and OVA airway challenge alone (3N).
Figure 3: AHR and BAL fluid cells in mice deficient in γδ or αβ T cells after 3-day airway challenge with OVA (3N treatment).
Figure 4: AHR and BAL fluid in TCR-depleted TCR-β–/– and TCR-δ–/– mice after 3 days of airway challenge with OVA (3N treatment).
Figure 5: Serum levels of OVA-specific immunoglobulins in C57BL/6, TCR-β–/– and TCR-δ–/– mice after 3N and 2ip3N treatments.
Figure 6: BAL fluid cytokine levels in C57BL/6, TCR-β–/– and TCR-δ–/– mice after 3N and 2ip3N treatments.
Figure 7: Effects of two different sensitization protocols (7ip3N and 2ip3N) on AHR and BAL fluid in C57BL/6, TCR-δ–/– and TCR-β–/– mice.

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Acknowledgements

We thank B. Schilling and L.Cunningham for their assistance in the histological preparation, and L. Landskroner for composing the illustrations. Salary support for M.L. was provided by the German Research Association (Deutsche Forschungsgemeinschaft), through a Postdoctoral Fellowship Award of the Arthritis Foundation and by the Melvin Garb Endowed Fellowship in Basic Immunology. This work was supported by NIH grants HL-36577 to E.W.G., AI-40611 to W.B. and AI-01291 to R.L.O., and by EPA grant R85793.

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Correspondence to Erwin W. Gelfand.

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Lahn, M., Kanehiro, A., Takeda, K. et al. Negative regulation of airway responsiveness that is dependent on γδ T cells and independent of αβ T cells. Nat Med 5, 1150–1156 (1999). https://doi.org/10.1038/13476

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