Phenotypic and functional analysis of EBV-specific memory CD8 cells in SLE

Elevated antinuclear antibodies and altered anti-Epstein-Barr virus immune responses

“…Specifically, a disruption in EBNA1 related antibodydependent cellular cytotoxicity and a reduced T cell cytotoxicity against EBV infected cells are noted in SLE (Rothfield et al, 1973;McClain et al, 2006). Additionally, EBV specific T cell cytotoxicity is also compromised in SLE patients (Berner et al, 2005).…”

Kikuchi-Fujimoto Disease and Systemic Lupus Erythematosus: The EBV Connection?

“…[19] Patients with KFD present with elevation of 2'-5'-oligoadenylate synthetase in the white blood cells and tubuloreticular structures in the histiocytes, activated lymphocytes, and endothelial cells. [13][14][15][16][17][18][19][20] These findings, strongly suggestive of hyperimmune response of viral etiology, have also been demonstrated in endothelial cells or lymphocytes of patients with SLE and other autoimmune disorders. [21] In conclusion, all of the above-mentioned data prompted us to hypothesize first that KFD and SLE could be two sides from the same coin of autoimmune disorders, the first being a milder manifestation of the latter, or two distinct autoimmune entities linked by the same pathogenetic factor, namely EBV infection.…”

“…[16] This has been attributed probably to altered T cell responses against EBV. [16,17] It has been demonstrated that the Epstein-Barr virus Nuclear Antigen-1 (EBNA-1) elicits the production of IgG antibodies to Sm and to doublestranded DNA. [18] Harley et al [19] found that the first lupus-specific autoantibodies are anti-Sm and anti-60 KD Ro and arise from particular autoantibodies against EBNA-1.…”

Epstein–Barr Virus and Autoimmunity: The Role of a Latent Viral Infection in Multiple Sclerosis and Systemic Lupus Erythematosus Pathogenesis

“…Early studies found that T cells from SLE patients were not as efficient as T cells from healthy controls in controlling EBV infection of autologous B cells [74]. Additionally, the decreased ability of EBV-specific CD8 + T cells to produce IFN-g was detected in SLE patients, suggesting that impaired control of EBV replication could be due to impaired EBV-specific CD8 + immunity [63,75].…”