| First Author | Antón IM | Year | 2002 |
| Journal | Immunity | Volume | 16 |
| Issue | 2 | Pages | 193-204 |
| PubMed ID | 11869681 | Mgi Jnum | J:74719 |
| Mgi Id | MGI:2159026 | Doi | 10.1016/s1074-7613(02)00268-6 |
| Citation | Anton IM, et al. (2002) WIP Deficiency Reveals a Differential Role for WIP and the Actin Cytoskeleton in T and B Cell Activation. Immunity 16(2):193-204 |
| abstractText | WIP stabilizes actin filaments and is important for filopodium formation. To define the role of WIP in immunity, we generated WIP-deficient mice. WIP(minus sign/minus sign) mice have normal lymphocyte development, but their T cells fail to proliferate, secrete IL-2, increase their F-actin content, polarize and extend protrusions following T cell receptor ligation, and are deficient in conjugate formation with superantigen-presenting B cells and anti-CD3 bilayers. In contrast, WIP-deficient B lymphocytes have enhanced proliferation and CD69 expression following B cell receptor ligation and mount normal antibody responses to T-independent antigens. Both WIP-deficient T and B cells show a profound defect in their subcortical actin filament networks. These results suggest that WIP is important for immunologic synapse formation and T cell activation. |
