TY  - JOUR
N1  - Copyright of this article belongs to American Association of Immunologists.
ID  - open1026
UR  - http://www.jimmunol.org/content/177/5/2793.full.pdf+html
IS  - 5
A1  - Wang, Hongsheng
A1  - Nicholas, Matilda W
A1  - Conway, Kara L
A1  - Sen, Pradip
A1  - Diz, Ramiro
A1  - Tisch, Roland M
A1  - Clarke, Stephen H
Y1  - 2006/09/01/
N2  - 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.
PB  - American Association of Immunologists
JF  - Journal of immunology (Baltimore, Md. : 1950)
VL  - 177
SN  - 0022-1767
TI  - EBV latent membrane protein 2A induces autoreactive B cell activation and TLR hypersensitivity.
SP  - 2793
AV  - restricted
EP  - 802
ER  -