Grant: Operating Grant

We have shown that the cell surface protein, CD34, is expressed by a number of cell types that play key roles in mucosal inflammation. We have also shown that deletion of the CD34 gene in mice renders them very resistant to asthma and a number of other inflammatory diseases. Interestingly, at steady state, these mice do not appear to suffer from any other obvious defects in the absence of this gene. We have also generated mice that express the human CD34 gene instead of the mouse gene and shown that these mice now regain their sensitivity to asthma. We are developing therapeutic strategies for interfering with human CD34 protein expression and evaluating their ability to inhibit disease. In addition, our data suggest that CD34 functions to enhance the ability of cells to migrate to tissues in response to inflammatory signals. Our goal with this application is to investigate this further and establish the basic mechanisms by which CD34 facilitates inflammatory migration in disease.