Nonhuman model animal lacking the ability to control lymphocyte migration

Abstract

The present invention provides a animal model useful in identifying a molecule controlling in a lymphocyte-specific manner migration and thus elucidating immune-related diseases and pathogenic conditions such as allergy, autoimmune diseases, GvH and graft rejections at a molecular level, or in developing a novel therapy. A nonhuman animal model such as a DOCK2 knockout mouse, in which the function to control lymphocyte migration has been deleted or suppressed, is generated by deleting DOCK2 gene on the chromosome. In this DOCK2 knockout mouse, the function of activating Rac to mediate actin cytoskeleton, the lymphocyte migration function in response: to stimuli with chemokines such as SLC, SDF-1, BLC, the homing function to secondary lymphoid organs such as spleen, lymph nodes and Peyer's patches, and the function of emigrating mature thymic T cells into peripheral blood in response to stimulus with chemokine ELC are impaired, and as a result of this, immune responses are suppressed.

1 - 23 . (canceled) 
     
     
         24 . A protein for controlling lymphocyte migration which mediates reorganization of cytoskeleton through activating Rac. 
     
     
         25 . The protein for controlling lymphocyte migration according to  claim 24 , wherein said protein is DOCK2 and a DOCK2 variant. 
     
     
         26 . The protein for controlling lymphocyte migration according to  claim 25 , wherein DOCK2 is an expression product of Hch gene (GenBank: accession No. AY027438). 
     
     
         27 . A method using the protein according to  claim 24  for controlling lymphocyte migration. 
     
     
         28 - 31 . (canceled)