WIP deficiency reveals a differential role for WIP and the actin cytoskeleton in T and B cell activation.

Journal article

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.

Authors: Antón, I; de la Fuente, MA; Sims, T; Freeman, S; Ramesh, N

• Journal: Immunity
• Volume: 16
• Issue: 2
• Pages: 193-204
• Publication date: 2002-02-01
• DOI: 10.1016/s1074-7613(02)00268-6
• EISSN: 1097-4180
• ISSN: 1074-7613
• Language: English
• Keywords: Immunoglobulin M; Cell Division; Actins; Carrier Proteins; Pseudopodia; Cells, Cultured; Receptors, Interleukin-2; Antigens, CD3; Mice, Knockout; Receptor-CD3 Complex, Antigen, T-Cell; Lymphocyte Activation; Cytoskeleton; T-Lymphocytes; Antigen-Presenting Cells; Immunoglobulin E; B-Lymphocytes; Mice; Animals