Immune responses to an early lytic cytomegalovirus antigen in systemic lupus erythematosus patients:  T-cell responses, cytokine secretions and antibody status

Anette Holck Draborg; Niclas Stefan Rasmussen; Janni Lisander Larsen; Charlotte Sværke Jørgensen; Noreen Sandhu; Kristin Skogstrand; Søren Jacobsen; Gunnar Houen; Jose C. Crispin

doi:10.1371/journal.pone.0193244

Immune responses to an early lytic cytomegalovirus antigen in systemic lupus erythematosus patients: T-cell responses, cytokine secretions and antibody status

Anette Holck Draborg, Niclas Stefan Rasmussen, Janni Lisander Larsen, Charlotte Sværke Jørgensen, Noreen Sandhu, Kristin Skogstrand, Søren Jacobsen, Gunnar Houen, Jose C. Crispin (Editor)

Department of Clinical Medicine

2 Citations (Scopus)

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Abstract

We investigated immune responses to a lytic cytomegalovirus antigen (CMVpp52), and to a lytic human herpes virus (HHV) 6 antigen (HHV6p41), in systemic lupus erythematosus (SLE) patients and healthy controls (HCs), in order to clarify if the previously established impaired responses to Epstein-Barr virus (EBV) in SLE patients is a general defect in their responses against (all) HHVs. Multiplex Luminex technology results showed a normal induction of five quantified cytokines (interferon γ, interleukin(IL)12, IL17, IL10, and tumor necrosis factor a) in SLE patients compared to HCs upon stimulation with CMVpp52 and HHV6p41. However, flow cytometric results showed a reduced upregulation of the activation marker CD69 on T-cells from SLE patients (n = 17) compared to HCs (n = 17) upon stimulation with CMVpp52, indicating limited or defective CMVpp52-specific T-cells and/or poor antigen-presentation in SLE patients, and thereby possibly decreased control of the CMV infection. In conclusion, the dysfunctional immune response against EBV previously established in SLE patients does not seem to apply to the same degree regarding the immune responses against CMV or HHV6. Results designate that the main contributing HHV agent in development or exacerbation of SLE (in genetically predisposed individuals) is the previously determined uncontrolled EBV infection, and to a lesser extent CMV infection, and probably with no involvement of HHV6 infection.

Original language	English
Article number	e0193244
Journal	PLOS ONE
Volume	13
Issue number	3
Number of pages	19
ISSN	1932-6203
DOIs	https://doi.org/10.1371/journal.pone.0193244
Publication status	Published - Mar 2018

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Draborg, A. H., Rasmussen, N. S., Larsen, J. L., Jørgensen, C. S., Sandhu, N., Skogstrand, K., Jacobsen, S., Houen, G., & Crispin, J. C. (Ed.) (2018). Immune responses to an early lytic cytomegalovirus antigen in systemic lupus erythematosus patients: T-cell responses, cytokine secretions and antibody status. PLOS ONE, 13(3), Article e0193244. https://doi.org/10.1371/journal.pone.0193244

Immune responses to an early lytic cytomegalovirus antigen in systemic lupus erythematosus patients: T-cell responses, cytokine secretions and antibody status. / Draborg, Anette Holck; Rasmussen, Niclas Stefan; Larsen, Janni Lisander et al.
In: PLOS ONE, Vol. 13, No. 3, e0193244, 03.2018.

Research output: Contribution to journal › Journal article › Research › peer-review

Draborg, AH, Rasmussen, NS, Larsen, JL, Jørgensen, CS, Sandhu, N, Skogstrand, K, Jacobsen, S, Houen, G & Crispin, JC (ed.) 2018, 'Immune responses to an early lytic cytomegalovirus antigen in systemic lupus erythematosus patients: T-cell responses, cytokine secretions and antibody status', PLOS ONE, vol. 13, no. 3, e0193244. https://doi.org/10.1371/journal.pone.0193244

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abstract = "We investigated immune responses to a lytic cytomegalovirus antigen (CMVpp52), and to a lytic human herpes virus (HHV) 6 antigen (HHV6p41), in systemic lupus erythematosus (SLE) patients and healthy controls (HCs), in order to clarify if the previously established impaired responses to Epstein-Barr virus (EBV) in SLE patients is a general defect in their responses against (all) HHVs. Multiplex Luminex technology results showed a normal induction of five quantified cytokines (interferon γ, interleukin(IL)12, IL17, IL10, and tumor necrosis factor a) in SLE patients compared to HCs upon stimulation with CMVpp52 and HHV6p41. However, flow cytometric results showed a reduced upregulation of the activation marker CD69 on T-cells from SLE patients (n = 17) compared to HCs (n = 17) upon stimulation with CMVpp52, indicating limited or defective CMVpp52-specific T-cells and/or poor antigen-presentation in SLE patients, and thereby possibly decreased control of the CMV infection. In conclusion, the dysfunctional immune response against EBV previously established in SLE patients does not seem to apply to the same degree regarding the immune responses against CMV or HHV6. Results designate that the main contributing HHV agent in development or exacerbation of SLE (in genetically predisposed individuals) is the previously determined uncontrolled EBV infection, and to a lesser extent CMV infection, and probably with no involvement of HHV6 infection.",

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AU - Larsen, Janni Lisander

AU - Jørgensen, Charlotte Sværke

AU - Sandhu, Noreen

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AB - We investigated immune responses to a lytic cytomegalovirus antigen (CMVpp52), and to a lytic human herpes virus (HHV) 6 antigen (HHV6p41), in systemic lupus erythematosus (SLE) patients and healthy controls (HCs), in order to clarify if the previously established impaired responses to Epstein-Barr virus (EBV) in SLE patients is a general defect in their responses against (all) HHVs. Multiplex Luminex technology results showed a normal induction of five quantified cytokines (interferon γ, interleukin(IL)12, IL17, IL10, and tumor necrosis factor a) in SLE patients compared to HCs upon stimulation with CMVpp52 and HHV6p41. However, flow cytometric results showed a reduced upregulation of the activation marker CD69 on T-cells from SLE patients (n = 17) compared to HCs (n = 17) upon stimulation with CMVpp52, indicating limited or defective CMVpp52-specific T-cells and/or poor antigen-presentation in SLE patients, and thereby possibly decreased control of the CMV infection. In conclusion, the dysfunctional immune response against EBV previously established in SLE patients does not seem to apply to the same degree regarding the immune responses against CMV or HHV6. Results designate that the main contributing HHV agent in development or exacerbation of SLE (in genetically predisposed individuals) is the previously determined uncontrolled EBV infection, and to a lesser extent CMV infection, and probably with no involvement of HHV6 infection.

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Immune responses to an early lytic cytomegalovirus antigen in systemic lupus erythematosus patients: T-cell responses, cytokine secretions and antibody status

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