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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


Division of Immunology, Children's Hospital and Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA.


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