Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

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.

Original publication




Journal article



Publication Date





193 - 204


Actins, Animals, Antigen-Presenting Cells, B-Lymphocytes, CD3 Complex, Carrier Proteins, Cell Division, Cells, Cultured, Cytoskeletal Proteins, Cytoskeleton, Immunoglobulin E, Immunoglobulin M, Lymphocyte Activation, Mice, Mice, Knockout, Pseudopodia, Receptor-CD3 Complex, Antigen, T-Cell, Receptors, Interleukin-2, T-Lymphocytes