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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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

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.[1]

References

  1. WIP deficiency reveals a differential role for WIP and the actin cytoskeleton in T and B cell activation. Antón, I.M., de la Fuente, M.A., Sims, T.N., Freeman, S., Ramesh, N., Hartwig, J.H., Dustin, M.L., Geha, R.S. Immunity (2002) [Pubmed]
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