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Reduced response to Epstein-Barr virus antigens by T-cells in systemic lupus erythematosus patients.

Draborg AH, Jacobsen S, Westergaard M, Mortensen S, Larsen JL, Houen G, Duus K - Lupus Sci Med (2014)

Bottom Line: Epstein-Barr virus (EBV) has for long been associated with systemic lupus erythematosus (SLE).These results indicate a limited or a defective EBV-specific T-cell response in SLE patients, which may suggest poor control of EBV infection in SLE with an immune reaction shift towards a humoral response in an attempt to control viral reactivation.A role for decreased control of EBV as a contributing agent in the development or exacerbation of SLE is proposed.

View Article: PubMed Central - PubMed

Affiliation: Department of Clinical Biochemistry, Immunology and Genetics , Statens Serum Institut , Copenhagen , Denmark.

ABSTRACT

Objective: Epstein-Barr virus (EBV) has for long been associated with systemic lupus erythematosus (SLE). In this study, we investigated the levels of latent and lytic antigen EBV-specific T-cells and antibodies in SLE patients.

Methods: T cells were analyzed by flow cytometry and antibodies were analyzed by enzyme-linked immunosorbent assay.

Results: SLE patients showed a significantly reduced number of activated (CD69) T-cells upon ex vivo stimulation with EBV nuclear antigen (EBNA) 1 or EBV early antigen diffuse (EBV-EA/D) in whole blood samples compared with healthy controls. Also, a reduced number of T-cells from SLE patients were found to produce interferon-γ upon stimulation with these antigens. Importantly, responses to a superantigen were normal in SLE patients. Compared with healthy controls, SLE patients had fewer EBV-specific T-cells but higher titres of antibodies against EBV. Furthermore, an inverse correlation was revealed between the number of lytic antigen EBV-specific T-cells and disease activity of the SLE patients, with high-activity SLE patients having fewer T-cells than low-activity SLE patients.

Conclusions: These results indicate a limited or a defective EBV-specific T-cell response in SLE patients, which may suggest poor control of EBV infection in SLE with an immune reaction shift towards a humoral response in an attempt to control viral reactivation. A role for decreased control of EBV as a contributing agent in the development or exacerbation of SLE is proposed.

No MeSH data available.


Related in: MedlinePlus

No difference in T-cell response between SLE patients and healthy controls upon superantigen stimulation. Heparinised whole blood samples from SLE patients (n=22) and sex-matched and age-matched healthy controls (n=22) were stimulated with SEB. Percentages of SEB-responding T-cells are presented as mean±SEM, and shows both CD69-expressing and IFN-γ-producing T-cells, and are divided into CD8 and CD4 (CD8−) T-cells. No statistical significant differences were found between SLE patients and healthy controls in either CD69-expressing cells or in IFN-γ-producing cells. SLE, systemic lupus erythematosus; SEB, staphylococcal enterotoxin B; IFN, interferon.
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LUPUS2014000015F4: No difference in T-cell response between SLE patients and healthy controls upon superantigen stimulation. Heparinised whole blood samples from SLE patients (n=22) and sex-matched and age-matched healthy controls (n=22) were stimulated with SEB. Percentages of SEB-responding T-cells are presented as mean±SEM, and shows both CD69-expressing and IFN-γ-producing T-cells, and are divided into CD8 and CD4 (CD8−) T-cells. No statistical significant differences were found between SLE patients and healthy controls in either CD69-expressing cells or in IFN-γ-producing cells. SLE, systemic lupus erythematosus; SEB, staphylococcal enterotoxin B; IFN, interferon.

Mentions: Importantly, no statistical significant differences were observed in either CD69 induction or IFN-γ production between SLE patients and HCs upon stimulation with the superantigen SEB (figure 4). Thus, the results achieved on EBNA1-specific and EBV-EA/D-specific T-cells are not a result of a general T-cell defect in the included SLE patients, although they tended to have slightly lower levels of activated T-cells.


Reduced response to Epstein-Barr virus antigens by T-cells in systemic lupus erythematosus patients.

Draborg AH, Jacobsen S, Westergaard M, Mortensen S, Larsen JL, Houen G, Duus K - Lupus Sci Med (2014)

No difference in T-cell response between SLE patients and healthy controls upon superantigen stimulation. Heparinised whole blood samples from SLE patients (n=22) and sex-matched and age-matched healthy controls (n=22) were stimulated with SEB. Percentages of SEB-responding T-cells are presented as mean±SEM, and shows both CD69-expressing and IFN-γ-producing T-cells, and are divided into CD8 and CD4 (CD8−) T-cells. No statistical significant differences were found between SLE patients and healthy controls in either CD69-expressing cells or in IFN-γ-producing cells. SLE, systemic lupus erythematosus; SEB, staphylococcal enterotoxin B; IFN, interferon.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4225738&req=5

LUPUS2014000015F4: No difference in T-cell response between SLE patients and healthy controls upon superantigen stimulation. Heparinised whole blood samples from SLE patients (n=22) and sex-matched and age-matched healthy controls (n=22) were stimulated with SEB. Percentages of SEB-responding T-cells are presented as mean±SEM, and shows both CD69-expressing and IFN-γ-producing T-cells, and are divided into CD8 and CD4 (CD8−) T-cells. No statistical significant differences were found between SLE patients and healthy controls in either CD69-expressing cells or in IFN-γ-producing cells. SLE, systemic lupus erythematosus; SEB, staphylococcal enterotoxin B; IFN, interferon.
Mentions: Importantly, no statistical significant differences were observed in either CD69 induction or IFN-γ production between SLE patients and HCs upon stimulation with the superantigen SEB (figure 4). Thus, the results achieved on EBNA1-specific and EBV-EA/D-specific T-cells are not a result of a general T-cell defect in the included SLE patients, although they tended to have slightly lower levels of activated T-cells.

Bottom Line: Epstein-Barr virus (EBV) has for long been associated with systemic lupus erythematosus (SLE).These results indicate a limited or a defective EBV-specific T-cell response in SLE patients, which may suggest poor control of EBV infection in SLE with an immune reaction shift towards a humoral response in an attempt to control viral reactivation.A role for decreased control of EBV as a contributing agent in the development or exacerbation of SLE is proposed.

View Article: PubMed Central - PubMed

Affiliation: Department of Clinical Biochemistry, Immunology and Genetics , Statens Serum Institut , Copenhagen , Denmark.

ABSTRACT

Objective: Epstein-Barr virus (EBV) has for long been associated with systemic lupus erythematosus (SLE). In this study, we investigated the levels of latent and lytic antigen EBV-specific T-cells and antibodies in SLE patients.

Methods: T cells were analyzed by flow cytometry and antibodies were analyzed by enzyme-linked immunosorbent assay.

Results: SLE patients showed a significantly reduced number of activated (CD69) T-cells upon ex vivo stimulation with EBV nuclear antigen (EBNA) 1 or EBV early antigen diffuse (EBV-EA/D) in whole blood samples compared with healthy controls. Also, a reduced number of T-cells from SLE patients were found to produce interferon-γ upon stimulation with these antigens. Importantly, responses to a superantigen were normal in SLE patients. Compared with healthy controls, SLE patients had fewer EBV-specific T-cells but higher titres of antibodies against EBV. Furthermore, an inverse correlation was revealed between the number of lytic antigen EBV-specific T-cells and disease activity of the SLE patients, with high-activity SLE patients having fewer T-cells than low-activity SLE patients.

Conclusions: These results indicate a limited or a defective EBV-specific T-cell response in SLE patients, which may suggest poor control of EBV infection in SLE with an immune reaction shift towards a humoral response in an attempt to control viral reactivation. A role for decreased control of EBV as a contributing agent in the development or exacerbation of SLE is proposed.

No MeSH data available.


Related in: MedlinePlus