{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,25]],"date-time":"2026-03-25T19:43:24Z","timestamp":1774467804176,"version":"3.50.1"},"reference-count":42,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2018,1,8]],"date-time":"2018-01-08T00:00:00Z","timestamp":1515369600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100000015","name":"Canadian Cancer Society Research Institute","doi-asserted-by":"publisher","award":["701936"],"award-info":[{"award-number":["701936"]}],"id":[{"id":"10.13039\/501100000015","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Biotech &amp;amp; Bioengineering"],"published-print":{"date-parts":[[2018,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:label\/><jats:p>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\u2013macrophage colony\u2010stimulating factor (GM\u2010CSF). GM\u2010CSF along with other pro\u2010inflammatory factors form a positive feedback loop that ultimately perpetuate the lesions. Hence, to engineer chemotaxis to GM\u2010CSF, we created a new chimeric GM\u2010CSF receptor alpha subunit (GMRchi) that was coupled with a previously engineered Ca<jats:sup>2+<\/jats:sup>\u2010activated RhoA. When these proteins were expressed in mammalian cells, it allowed migration to chemical and cellular sources of GM\u2010CSF. As a possible therapeutic intervention, we further implemented the mechanism of cell\u2013cell membrane fusion and subsequent death. Since the microenvironment of lesions is more than just GM\u2010CSF 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\u2010based therapy of autoimmune lesions.<\/jats:p><\/jats:sec>","DOI":"10.1002\/bit.26523","type":"journal-article","created":{"date-parts":[[2017,12,18]],"date-time":"2017-12-18T07:55:25Z","timestamp":1513583725000},"page":"1028-1036","source":"Crossref","is-referenced-by-count":7,"title":["Engineered cell migration to lesions linked to autoimmune disease"],"prefix":"10.1002","volume":"115","author":[{"given":"Abdullah Al","family":"Mosabbir","sequence":"first","affiliation":[{"name":"Institute of Biomaterials and Biomedical Engineering University of Toronto Toronto, Ontario Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anam","family":"Qudrat","sequence":"additional","affiliation":[{"name":"Institute of Biomaterials and Biomedical Engineering University of Toronto Toronto, Ontario Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9520-2144","authenticated-orcid":false,"given":"Kevin","family":"Truong","sequence":"additional","affiliation":[{"name":"Institute of Biomaterials and Biomedical Engineering University of Toronto Toronto, Ontario Canada"},{"name":"Edward S. 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