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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 α) 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 publication




Journal article


PLoS One

Publication Date





Adult, Aged, Aged, 80 and over, Antibodies, Viral, Antigens, CD, Antigens, Differentiation, T-Lymphocyte, Antigens, Viral, Case-Control Studies, Cytokines, Cytomegalovirus, DNA-Binding Proteins, Enzyme-Linked Immunosorbent Assay, Female, Herpesvirus 6, Human, Humans, Immediate-Early Proteins, Lectins, C-Type, Lupus Erythematosus, Systemic, Male, Middle Aged, T-Lymphocytes, Viral Proteins, Young Adult