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Blood, 15 August 2001, Vol. 98, No. 4, pp. 1086-1094
IMMUNOBIOLOGY
Cdc42, Rac1, and the Wiskott-Aldrich syndrome protein are
involved in the cytoskeletal regulation of B lymphocytes
Lisa Westerberg,
Gediminas Greicius,
Scott B. Snapper,
Pontus Aspenström, and
Eva Severinson
From the Department of Cell and Molecular Biology,
Karolinska Institutet, Stockholm; the Ludwig Institute of Cancer
Research, Biomedical Center, Uppsala, Sweden; and the Gastrointestinal
Unit, Massachusetts General Hospital, Boston, MA.
Patients with the immunodeficiency disorder Wiskott-Aldrich
syndrome (WAS) have lymphocytes with aberrant microvilli, and their T
cells, macrophages, and dendritic cells are impaired in cytoskeletal-dependent processes. WAS is caused by a defective or a
missing WAS protein (WASP). Signal mediators interleukin-4 (IL-4) and
CD40 are important for actin-dependent morphology changes in B cells. A
possible function of WASP and its interacting partners, Cdc42 and Rac1,
was investigated for these changes. It was found that active Cdc42 and
Rac1 induced filopodia and lamellipodia, respectively, in activated B
cells. Evidence is given that IL-4 has a specific role in the regulated
cycling of Cdc42 because IL-4 partially and transiently depleted active
Cdc42 from detergent extract of activated B cells. WASP-deficient B
lymphocytes were impaired in IL-4- and CD40-dependent induction of
polarized and spread cells. Microvilli were expressed on WASP-deficient
B cells, but they appeared shorter and less dense in cell contacts than in wild-type cells. In conclusion, evidence is provided for the involvement of Cdc42, Rac1, and WASP in the cytoskeletal regulation of
B lymphocytes. Aberrations in WASP-deficient B lymphocytes, described
here, provide further evidence that WAS is a cytoskeletal disease of
hematopoietic cells.
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