RT info:eu-repo/semantics/article
T1 WIP deficiency reveals a differential role for WIP and the actin cytoskeleton in T and B cell activation
A1 Antón, Inés María
A1 Fuente García, Miguel Ángel de la
A1 Sims, Tasha N.
A1 Freeman, Sheryl
A1 Ramesh, Narayanaswamy
A1 Hartwig, John H.
A1 Dustin, Michael L.
A1 Geha, Raif S.
K1 Biología celular
AB 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.
PB Elsevier (Cell Press)
SN 1074-7613
YR 2002
FD 2002
LK http://uvadoc.uva.es/handle/10324/10144
UL http://uvadoc.uva.es/handle/10324/10144
LA eng
NO Immunity, 2002, 16(2):193-204
NO Producción Científica
DS UVaDOC
RD 23-dic-2024