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Latent Membrane Protein 1, the EBV-encoded oncogenic mimic of CD40, accelerates autoimmunity in B6.Sle1 mice
Journal article   Peer reviewed

Latent Membrane Protein 1, the EBV-encoded oncogenic mimic of CD40, accelerates autoimmunity in B6.Sle1 mice

Anna L Peters, Laura L Stunz, David K Meyerholz, Chandra Mohan and Gail A Bishop
The Journal of immunology (1950), Vol.185(7), pp.4053-4062
10/01/2010
DOI: 10.4049/jimmunol.0904065
PMCID: PMC3048355
PMID: 20810985

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Abstract

EBV infection is associated with development of the autoimmune disease systemic lupus erythematosus (SLE), and EBV can reactivate during SLE flares. Latent membrane protein-1 (LMP1) is an EBV-encoded, oncogenic mimic of CD40 that can be re-expressed in PBMCs during SLE flares, as >90% of humans are latently EBV-infected. Whether LMP1 signaling exacerbates SLE is unknown. The phenotype of mice expressing a chimeric molecule with the mouse CD40 extracellular domain and the LMP1 intracellular signaling regions (mCD40-LMP1tg) includes enhanced autoreactivity, yet these mice do not develop fatal autoimmune disease. We hypothesized that LMP1-mediated activation signals cooperate with and/or amplify events that predispose individuals to development of autoimmunity. To determine which aspects of autoimmunity may be exacerbated by LMP1, we bred mCD40-LMP1tg mice to two lupus-prone strains, B6.Sle1 and B6.Sle3, and analyzed autoimmunity parameters. LMP1 + Sle1 +/+ mice developed enlarged lymphoid organs containing increased frequencies of germinal center, B cells, CD86 + B cells, and activated and memory T cells compared to non-transgenic littermates. Anti-histone antibodies were elevated in serum of LMP1 + Sle1 +/+ mice, and they had signs of kidney pathology. LMP1 + Sle1 +/+ B cells produced increased IL-6 and upregulated CD86 to a higher degree following CD40 stimulation in vitro , suggesting that the in vivo autoimmune exacerbation is B-cell intrinsic. In contrast, the LMP1 transgene has no additional effects on autoimmunity on the B6.Sle3 background. These data indicate that LMP1-induced effects can cooperate with distinct subsets of host genes that predispose to autoimmunity, and can thus be an exacerbating factor in autoimmune disease via multiple mechanisms.
systemic lupus erythematosus B cells autoimmunity autoantibodies

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