| First Author | Caldwell RG | Year | 1998 |
| Journal | Immunity | Volume | 9 |
| Issue | 3 | Pages | 405-11 |
| PubMed ID | 9768760 | Mgi Jnum | J:129571 |
| Mgi Id | MGI:3769753 | Doi | 10.1016/s1074-7613(00)80623-8 |
| Citation | Caldwell RG, et al. (1998) Epstein-Barr virus LMP2A drives B cell development and survival in the absence of normal B cell receptor signals. Immunity 9(3):405-11 |
| abstractText | Epstein-Barr virus (EBV) establishes a persistent latent infection in peripheral B lymphocytes in humans and is associated with a variety of malignancies and proliferative disorders. Latent membrane protein 2A (LMP2A) is one of only two viral proteins expressed in latently infected B lymphocytes in vivo. LMP2A blocks B cell receptor (BCR) signal transduction in vitro by binding the Syk and Lyn protein tyrosine kinases. To analyze the significance of LMP2A expression in vivo, transgenic mice with B cell lineage expression of LMP2A were generated. LMP2A expression results in the bypass of normal B lymphocyte developmental checkpoints allowing immunoglobulin-negative cells to colonize peripheral lymphoid organs, indicating that LMP2A possesses a constitutive signaling activity in nontransformed cells. |
