DOCK2 controls lymphocyte migration

The exit of lymphocytes from the vasculature is essential for the control of the inflammatory response. Cell migration involves cytoskeletal dynamics controlled by Rac GTPases but the full molecular mechanism remains unknown. In August 23 Nature, Yoshinori Fukui and colleagues from Kyushu University, Japan, show that DOCK2, a haematopoietic cell-specific protein, mediates cytoskeletal reorganization via Rac activation and is indispensable for lymphocyte chemotaxis.Fukui et al. studied DOCK2-defc

Tudor Toma(t.toma@ic.ac.uk)
Aug 27, 2001

The exit of lymphocytes from the vasculature is essential for the control of the inflammatory response. Cell migration involves cytoskeletal dynamics controlled by Rac GTPases but the full molecular mechanism remains unknown. In August 23 Nature, Yoshinori Fukui and colleagues from Kyushu University, Japan, show that DOCK2, a haematopoietic cell-specific protein, mediates cytoskeletal reorganization via Rac activation and is indispensable for lymphocyte chemotaxis.

Fukui et al. studied DOCK2-defcient mice (DOCK2-/-) and found that these mice exhibited migration defects of T- and B-lymphocytes in response to chemokines, while the monocyte migration was unaffected. This resulted in several abnormalities including T lymphocytopenia, atrophy of lymphoid follicles and loss of marginal-zone B cells. In DOCK2-/- lymphocytes, chemokine-induced Rac activation and actin polymerization were almost totally abolished, showing that DOCK2 function via Rac activation (Nature 2001, 412:826-831).

These results confirm that of lymphocyte and monocyte migration...

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