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Corticosteroids and infliximab impair the performance of interferon-γ release assays used for diagnosis of latent tuberculosis

Corticosteroids and infliximab impair the performance of interferon-γ release assays used for diagnosis of latent tuberculosis
Corticosteroids and infliximab impair the performance of interferon-γ release assays used for diagnosis of latent tuberculosis
The impact of immunosuppression on interferon-γ release assays and novel cytokine biomarkers of TB infection, mycobacteria-specific IL-2, IP-10 and TNF-α responses was investigated in an ex vivo model. Cytokine responses in standard QuantiFERON-TB Gold in-Tube (QFT-GIT) assays were compared with duplicate assays containing dexamethasone or infliximab. Dexamethasone converted QFT-GIT results from positive to negative in 30% of participants. Antigen-stimulated interferon-γ, IL-2 and TNF-α responses were markedly reduced, but IP-10 responses were preserved. Infliximab caused QFT-GIT result conversion in up to 30% of participants and substantial reductions in all cytokine responses. Therefore, corticosteroids and anti-TNF-α agents significantly impair interferon-γ release assay performance. IP-10 may be a more robust TB biomarker than interferon-γ in patients receiving corticosteroids.
0040-6376
Edwards, Alexander
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Gao, Yifang
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Allan, Raymond
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Ball, Darran
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De Graaf, Hans
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Coelho, Tracy
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Clifford, Vanessa
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Curtis, Nigel
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Williams, Tony
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Faust, Saul
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Mansour, Salah
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Marshall, Ben
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Elkington, Paul
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Tebruegge, Marc
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Edwards, Alexander
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Gao, Yifang
eea234ba-f566-4f21-a65e-234b84cba285
Allan, Raymond
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Ball, Darran
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De Graaf, Hans
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Coelho, Tracy
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Clifford, Vanessa
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Curtis, Nigel
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Williams, Tony
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Faust, Saul
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Mansour, Salah
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Marshall, Ben
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Elkington, Paul
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Tebruegge, Marc
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Edwards, Alexander, Gao, Yifang, Allan, Raymond, Ball, Darran, De Graaf, Hans, Coelho, Tracy, Clifford, Vanessa, Curtis, Nigel, Williams, Tony, Faust, Saul, Mansour, Salah, Marshall, Ben, Elkington, Paul and Tebruegge, Marc (2017) Corticosteroids and infliximab impair the performance of interferon-γ release assays used for diagnosis of latent tuberculosis. Thorax. (doi:10.1136/thoraxjnl-2016-209397). (PMID:28159773)

Record type: Article

Abstract

The impact of immunosuppression on interferon-γ release assays and novel cytokine biomarkers of TB infection, mycobacteria-specific IL-2, IP-10 and TNF-α responses was investigated in an ex vivo model. Cytokine responses in standard QuantiFERON-TB Gold in-Tube (QFT-GIT) assays were compared with duplicate assays containing dexamethasone or infliximab. Dexamethasone converted QFT-GIT results from positive to negative in 30% of participants. Antigen-stimulated interferon-γ, IL-2 and TNF-α responses were markedly reduced, but IP-10 responses were preserved. Infliximab caused QFT-GIT result conversion in up to 30% of participants and substantial reductions in all cytokine responses. Therefore, corticosteroids and anti-TNF-α agents significantly impair interferon-γ release assay performance. IP-10 may be a more robust TB biomarker than interferon-γ in patients receiving corticosteroids.

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Tebruegge et al - Eprints - Impact of immunosuppressive agents on IGRA performance - combined.pdf - Accepted Manuscript
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Accepted/In Press date: 12 January 2017
e-pub ahead of print date: 3 February 2017
Organisations: Clinical & Experimental Sciences

Identifiers

Local EPrints ID: 405831
URI: http://eprints.soton.ac.uk/id/eprint/405831
ISSN: 0040-6376
PURE UUID: 9df87fee-c73b-4da4-9b71-d777515f7794
ORCID for Saul Faust: ORCID iD orcid.org/0000-0003-3410-7642
ORCID for Salah Mansour: ORCID iD orcid.org/0000-0002-5982-734X
ORCID for Paul Elkington: ORCID iD orcid.org/0000-0003-0390-0613

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Date deposited: 18 Feb 2017 00:19
Last modified: 16 Mar 2024 04:11

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Contributors

Author: Alexander Edwards
Author: Yifang Gao
Author: Raymond Allan
Author: Darran Ball
Author: Hans De Graaf
Author: Tracy Coelho
Author: Vanessa Clifford
Author: Nigel Curtis
Author: Tony Williams
Author: Saul Faust ORCID iD
Author: Salah Mansour ORCID iD
Author: Ben Marshall
Author: Paul Elkington ORCID iD
Author: Marc Tebruegge

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