Americas Committee for Treatment and Research in Multiple Sclerosis
West Palm Beach, Florida


How Can IL-13 Be Applied Toward Neuroprotection in Multiple Sclerosis?

Chloé Hoornaert, PhD, from the Department of Neuroscience at the University of Montreal Hospital Research Centre in Montreal, Quebec, presented evidence that the anti-inflammatory cytokine IL-13 may have neuroprotective qualities in MS.WEST PALM BEACH, FL — Current treatments for neurologic diseases involve "extensive and forcible suppression" of immune cells. Instead, therapeutic approaches "should move toward careful adjustment of the balance between their different phenotypes," suggested University of Montreal researcher Chloé Hoornaert, PhD.

In the "Groundbreaking Abstracts" session at the ACTRIMS Forum on Friday, February 28, Dr. Hoornaert, from the University of Montreal Hospital Research Centre in Quebec, described her work with interleukin-13 (IL-13). IL-13 is an anti-inflammatory cytokine predominantly secreted by T helper type 2 (Th2) cells, but also by CD4, Natural killer cells, and others. "IL-13 is a well-known modulator of immune responses in vitro and in vivo, with potential neuroprotective properties, as demonstrated in several experimental models of neurodegenerative disorders," Dr. Hoornaert said. Previous work has shown that IL-13 strongly decreases pro-inflammatory cytokine secretion, reduces inflammatory cell infiltration, and suppresses axonal loss.

To learn more about the potential for IL-13 in MS, Dr. Hoornaert sought to find out:

  • How does IL-13 behave at the level of the blood brain barrier (BBB)?
  • What is the effect of IL-13 signaling on immune cells? Which circulating immune cells are the predominant responders to IL-13?
  • Does IL-13 signaling regulate cellular adhesion molecule expression on immune cells?

To summarize her findings, she noted that in the blood compartments, CD14-positive monocytes are the predominant cells that express the receptor for IL-13. IL-13 treatment was shown to increase expression of various cell adhesion molecules on their surfaces. IL-13 induces VCAM1 expression on both human endothelial and human meningeal cells and increases leukocyte migration across resting meningeal barriers. And IL-13 tightens BBB and blood-meningeal barrier function in both their resting and inflamed conditions.

Previous research by Dr. Hoornaert and colleagues with IL-13 involved a mouse model of ischemic stroke, in an effort to drive microglia and macrophages toward a more protective, anti-inflammatory effect on the nerve cells. In a study published in 2018, the group reported that transplanting IL13-expressing mesenchymal stem cells (MSCs) into the animals following ischemic stroke led to targeted intracerebral delivery of IL-13. This promoted a phenotypic switch of microglia and macrophages during the pro-inflammatory phase. Other research by this group has involved transplant of IL-13-expressing MSCs in models of spinal cord injury.


By Katherine Wandersee, for the Consortium of Multiple Sclerosis Centers (CMSC)


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