Functional inactivation of CXCR4-mediated responses in growth hormone transgenic mice through SOCS3 upregulation

Abstract

The present invention permits data, derived from bGH-Tg mice in the context of crosstalk between cytokine and chemokine responses, to aid in understanding the functional role of this chemokine/chemokine receptor pair. As the only models available to date were thoses in which the CXCR4 or CXCL12 deletion is lethal before birth the present invention provides means for relating cytokine-mediated effects to the functional role of CXCR4 inactivation in postanatal life. A method is provided for treating a human having a disease associated with CXCR4-dependent HIV comprising administering to said human a therapeutically anti-viral effective amount of a molecule that induces the expression of SOCS3 and a pharmaceutically acceptable carrier. A method is provided for treating a human having a disease associated with CXCR4-dependent HIV, wherein said molecule binds to GHR.