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IL-4 increases type 2, but not type 1, cytokine production in CD8+ T cells from mild atopic asthmatics

IL-4 increases type 2, but not type 1, cytokine production in CD8+ T cells from mild atopic asthmatics
IL-4 increases type 2, but not type 1, cytokine production in CD8+ T cells from mild atopic asthmatics
Background: Virus infections are the major cause of asthma exacerbations. CD8+ T cells have an important role in antiviral immune responses and animal studies suggest a role for CD8+ T cells in the pathogenesis of virus-induced asthma exacerbations. We have previously shown that the presence of IL-4 during stimulation increases the frequency of IL-5-positive cells and CD30 surface staining in CD8+ T cells from healthy, normal subjects. In this study, we investigated whether excess IL-4 during repeated TCR/CD3 stimulation of CD8+ T cells from atopic asthmatic subjects alters the balance of type 1/type 2 cytokine production in favour of the latter.
Methods: Peripheral blood CD8+ T cells from mild atopic asthmatic subjects were stimulated in vitro with anti-CD3 and IL-2 ± excess IL-4 and the expression of activation and adhesion molecules and type 1 and type 2 cytokine production were assessed.
Results: Surface expression of very late antigen-4 [VLA-4] and LFA-1 was decreased and the production of the type 2 cytokines IL-5 and IL-13 was augmented by the presence of IL-4 during stimulation of CD8+ T cells from mild atopic asthmatics.
Conclusion: These data suggest that during a respiratory virus infection activated CD8+ T cells from asthmatic subjects may produce excess type 2 cytokines and may contribute to asthma exacerbation by augmenting allergic inflammation.
1465-9921
67
Stanciu, Luminita A.
92eb55fa-d20e-4d3a-aa71-207eaf6bceca
Roberts, Kevan
2cf2d2f6-7911-41f9-a03e-5cf7735d7480
Papadopoulos, Nikolaos G.
bb0da82a-300e-44b9-ba26-3573d81f48be
Cho, Sang-Heon
1fe9b7ee-da4d-4a4c-ad6c-16b3269f4610
Holgate, Stephen T.
2e7c17a9-6796-436e-8772-1fe6d2ac5edc
Coyle, Anthony J.
1aad12d1-d2d3-48e5-b3fc-1e31d7e9c1a4
Johnston, Sebastian L.
90e0ef79-cfde-40e0-b301-90d3063ee036
Stanciu, Luminita A.
92eb55fa-d20e-4d3a-aa71-207eaf6bceca
Roberts, Kevan
2cf2d2f6-7911-41f9-a03e-5cf7735d7480
Papadopoulos, Nikolaos G.
bb0da82a-300e-44b9-ba26-3573d81f48be
Cho, Sang-Heon
1fe9b7ee-da4d-4a4c-ad6c-16b3269f4610
Holgate, Stephen T.
2e7c17a9-6796-436e-8772-1fe6d2ac5edc
Coyle, Anthony J.
1aad12d1-d2d3-48e5-b3fc-1e31d7e9c1a4
Johnston, Sebastian L.
90e0ef79-cfde-40e0-b301-90d3063ee036

Stanciu, Luminita A., Roberts, Kevan, Papadopoulos, Nikolaos G., Cho, Sang-Heon, Holgate, Stephen T., Coyle, Anthony J. and Johnston, Sebastian L. (2005) IL-4 increases type 2, but not type 1, cytokine production in CD8+ T cells from mild atopic asthmatics. Respiratory Research, 6 (1), 67. (doi:10.1186/1465-9921-6-67).

Record type: Article

Abstract

Background: Virus infections are the major cause of asthma exacerbations. CD8+ T cells have an important role in antiviral immune responses and animal studies suggest a role for CD8+ T cells in the pathogenesis of virus-induced asthma exacerbations. We have previously shown that the presence of IL-4 during stimulation increases the frequency of IL-5-positive cells and CD30 surface staining in CD8+ T cells from healthy, normal subjects. In this study, we investigated whether excess IL-4 during repeated TCR/CD3 stimulation of CD8+ T cells from atopic asthmatic subjects alters the balance of type 1/type 2 cytokine production in favour of the latter.
Methods: Peripheral blood CD8+ T cells from mild atopic asthmatic subjects were stimulated in vitro with anti-CD3 and IL-2 ± excess IL-4 and the expression of activation and adhesion molecules and type 1 and type 2 cytokine production were assessed.
Results: Surface expression of very late antigen-4 [VLA-4] and LFA-1 was decreased and the production of the type 2 cytokines IL-5 and IL-13 was augmented by the presence of IL-4 during stimulation of CD8+ T cells from mild atopic asthmatics.
Conclusion: These data suggest that during a respiratory virus infection activated CD8+ T cells from asthmatic subjects may produce excess type 2 cytokines and may contribute to asthma exacerbation by augmenting allergic inflammation.

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Published date: 2005

Identifiers

Local EPrints ID: 27437
URI: http://eprints.soton.ac.uk/id/eprint/27437
ISSN: 1465-9921
PURE UUID: ce9a8218-4973-4be4-b0e5-a390c91a45ce

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Date deposited: 27 Apr 2006
Last modified: 15 Mar 2024 07:18

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Contributors

Author: Luminita A. Stanciu
Author: Kevan Roberts
Author: Nikolaos G. Papadopoulos
Author: Sang-Heon Cho
Author: Anthony J. Coyle
Author: Sebastian L. Johnston

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