Redirecting adult mesenchymal stromal cells to the brain: a new approach for treating CNS autoimmunity and neuroinflammation?

Autor: Wilson JJ; The Chemokine Biology Laboratory, The University of Adelaide, Adelaide, SA, 5005, Australia., Foyle KL; The Chemokine Biology Laboratory, The University of Adelaide, Adelaide, SA, 5005, Australia., Foeng J; The Chemokine Biology Laboratory, The University of Adelaide, Adelaide, SA, 5005, Australia., Norton T; The Chemokine Biology Laboratory, The University of Adelaide, Adelaide, SA, 5005, Australia., McKenzie DR; The Chemokine Biology Laboratory, The University of Adelaide, Adelaide, SA, 5005, Australia., Payne N; Multiple Sclerosis Research Group, Australian Regenerative Medicine Institute, Monash University, Clayton, VIC, 3800, Australia., Bernard CC; Multiple Sclerosis Research Group, Australian Regenerative Medicine Institute, Monash University, Clayton, VIC, 3800, Australia., McColl SR; The Chemokine Biology Laboratory, The University of Adelaide, Adelaide, SA, 5005, Australia., Comerford I; The Chemokine Biology Laboratory, The University of Adelaide, Adelaide, SA, 5005, Australia.
Jazyk: angličtina
Zdroj: Immunology and cell biology [Immunol Cell Biol] 2018 Apr; Vol. 96 (4), pp. 347-357. Date of Electronic Publication: 2018 Mar 02.
DOI: 10.1111/imcb.12014
Abstrakt: Mesenchymal stromal cells or stem cells (MSCs) have been shown to participate in tissue repair and are immunomodulatory in neuropathological settings. Given this, their potential use in developing a new generation of personalized therapies for autoimmune and inflammatory diseases of the central nervous system (CNS) will be explored. To effectively exert these effector functions, MSCs must first gain entry into damaged neural tissues, a process that has been demonstrated to be a limiting factor in their therapeutic efficacy. In this review, we discuss approaches to maximize the therapeutic efficacy of MSCs by altering their intrinsic trafficking programs to effectively enter neuropathological sites. To this end, we explore the significant role of chemokine receptors and adhesion molecules in directing cellular traffic to the inflamed CNS and the capacity of MSCs to adopt these molecular mechanisms to gain entry to this site. We postulate that understanding and exploiting these migratory mechanisms may be key to the development of cell-based therapies tailored to respond to the migratory cues unique to the nature and stage of progression of individual CNS disorders.
(© 2018 Australasian Society for Immunology Inc.)
Databáze: MEDLINE
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