Ebv Latent Membrane Protein 2a Induces Autoreactive B Cell Activation and Tlr Hypersensitivity.
From: Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, NC 27599, USA.
Journal of immunology (Baltimore, Md. : 1950)
- Publish Date: Sep 2006
- ISSN: 0022-1767
- Volume: 177
- Issue: 5
- Pages: 2793-802
- Medium: Print
- Language: English
- Citation (JAMA): Wang Hongsheng, Nicholas Matilda W, Conway Kara L, et al. Ebv Latent Membrane Protein 2a Induces Autoreactive B Cell Activation and Tlr Hypersensitivity.. J. Immunol. Sep 2006;177:2793-802
Abstract
EBV is associated with systemic lupus erythematosus (SLE), but how it might contribute to the etiology is not clear. Since EBV-encoded latent membrane protein 2A (LMP2A) interferes with normal B cell differentiation and function, we sought to determine its effect on B cell tolerance. Mice transgenic for both LMP2A and the Ig transgene 2-12H specific for the ribonucleoprotein Smith (Sm), a target of the immune system in SLE, develop a spontaneous anti-Sm response. LMP2A allows anti-Sm B cells to overcome the regulatory checkpoint at the early preplasma cell stage by a self-Ag-dependent mechanism. LMP2A induces a heightened sensitivity to TLR ligand stimulation, resulting in increased proliferation or Ab-secreting cell differentiation or both. Thus, we propose a model whereby LMP2A induces hypersensitivity to TLR stimulation, leading to activation of anti-Sm B cells through the BCR/TLR pathway. These data further implicate TLRs in the etiology of SLE and suggest a mechanistic link between EBV infection and SLE.
Mesh Headings (Keywords): Animals, B-Lymphocytes, Cell Differentiation, Cell Movement, Cell Proliferation, Hypersensitivity, Lymphocyte Activation, Mice, Mice, Transgenic, NF-kappa B, Phenotype, Ribonucleoproteins, Spleen, Toll-Like Receptors, Viral Matrix Proteins
Check for Full Text / PubMed Unique Identifier (PMID): 16920914
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