Abstract: The present invention pertains to the treatment of diseases inducing or resulting from an abnormal immune response within a body tissue. The present inventors have demonstrated that S1PR2 engagement inhibits chemokine-induced migration of memory T cell subsets. The S1PR2-mediated pathway thus allows for the retention of T cells within a tissue. The inhibition of such a pathway by using selective S1PR2 inhibitors thus represents a promising alternative for the local treatment of several inflammatory diseases. Accordingly, the present invention pertains to a selective antagonist of S1PR2 for use in the treatment of diseases inducing or resulting from an abnormal immune response within a body tissue. The selective antagonist of S1PR2 is administered topically to the tissue in which the abnormal immune response occurs.

Abstract: The present invention relates to expression constructs and methods of specifically marking NK cells in nonhuman mammals. Specifically, methods are presented that allow the specific expression of foreign genes in the NK cells of a nonhuman mammal. Such methods are useful for the generation of animal models for disorders involving NK cells, and for the evaluation of genes or compounds with respect to their effects on NK cells.