The damaging and degenerative effects in autoimmune diseases such as rheumatoid arthritis， multiple sclerosis and Crohn's disease often manifests as the formation of lesions that feature a high local concentration of granulocyte-macrophage colony-stimulating factor (GM-CSF). GM-CSF along with other pro-inflammatory factors form a positive feedback loop that ultimately perpetuate the lesions. Hence， to engineer chemotaxis to GM-CSF， we created a new chimeric GM-CSF receptor alpha subunit (GMRchi) that was coupled with a previously engineered Ca -activated RhoA. When these proteins were expressed in mammalian cells， it allowed migration to chemical and cellular sources of GM-CSF. As a possible therapeutic intervention， we further implemented the mechanism of cell-cell membrane fusion and subsequent death. Since the microenvironment of lesions is more than just GM-CSF secretion， the further ability to recognize a combination of other features such as tissue markers will be needed for greater specificity. Nonetheless， this work represents a first step to enable cell-based therapy of autoimmune lesions.